Epidemiology

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Etiology

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Pathophysiology

• Neurogenic symptoms are mediated via norepinephrine/epinephrine and acetylcholine release during sytimpathec stimulation. Symptoms due to norepinephrine/epinephrine include tremulousness, tachycardia, and anxiety/arousal, whereas acetylcholine causes sweating, hunger, and paresthesias.
• Neuroglycopenic symptoms are due to inadequate availability of glucose in the CNS and include behavioral changes, confusion, visual disturbances, stupor, and seizures.

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Clinical features

• Beta blockers can mask signs of hypoglycemia.
  • Nonselective beta blockers attenuate the norepinephrine/epinephrine-mediated symptoms of hypoglycemia, but cholinergic symptoms (eg, hunger) are unaffected.
  • In addition, nonselective beta blockers can contribute to the severity of hypoglycemia; epinephrine stimulates hepatic gluconeogenesis and peripheral glycogenolysis, but this effect is diminished by nonselective beta blockers.

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Diagnostics

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Treatment

• Alert and oriented patients
  • Oral glucose 15–20 g
  • Fast-acting carbohydrates (e.g., glucose tablets, candy, or fruit juice)
• Patients with altered mental status (or impaired oral intake)
  • IV dextrose (e.g., D50W): Repeat after 15 minutes if hypoglycemia persists; multiple doses may be required.
    • Adults: 50% dextrose
    • Children (excluding neonates): 10% dextrose OR 25% dextrose
  • IM glucagon: if neither oral nor IV routes of administering glucose are feasible
    • Glucagon therapy is only successful if the patient’s glycogen reserves have not been depleted, as glucagon elevates endogenous glucose production via hepatic glycogenolysis and gluconeogenesis.

Tip

For patients with type 1 diabetes presenting with hypoglycemia and using insulin pumps, do not discontinue insulin pumps and treat hypoglycemia as usual. Removing the insulin pump puts patients at risk for diabetic ketoacidosis.

Warning

Avoid giving orange juice to patients with CKD on a low-potassium diet as it is high in potassium.

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