Diabetes Mellitus, Juvenile



  • Decrease in effective circulating insulin
  • Increase in counter-regulatory hormones including glucagon, catecholamines, cortisol, and growth hormone
  • Hyperglycemia owing to:
    • Decreased peripheral glucose utilization
    • Increased hepatic gluconeogenesis
  • Hyperosmolality and osmotic diuresis due to hyperglycemia
  • Ketoacidosis produced by increased lipolysis, with ketone body (β-hydroxybutyrate, acetoacetate) production, causes ketonemia and metabolic acidosis, which is augmented with lactic acidosis from poor tissue perfusion
  • Potassium deficit:
    • Intracellular shifts into extracellular space owing to hydrogen ion exchange
    • Loss from osmotic diuresis


  • Immune-mediated pancreatic islet β-cell destruction
  • The overall incidence has been increased worldwide by 2–5% over the past 20 yr
  • Precipitating events leading to diabetic ketoacidosis (DKA):
    • Infection, often minor acute illness such as virus, group A streptococcal pharyngitis, or UTI
    • Stress
    • Endocrine: Pregnancy, puberty, hyperthyroidism
    • Psychiatric disorders, including eating disorders
    • Medication noncompliance, inappropriate interruption of insulin pump therapy, or treatment error
  • Risk factors for cerebral edema associated with DKA:
    • Attenuated rise in measured serum sodium during DKA therapy (unrelated to the volume or sodium content of IV fluid or rate of change in serum glucose)
    • Bicarbonate treatment for acidosis correction
    • Hypocapnia
    • Increased serum urea nitrogen
    • No association with degree of hyperglycemia
    • Demographic factors that have been associated with an increased risk of cerebral edema include younger age, longer duration of symptoms, and new onset diabetes mellitus. These factors are also associated with increased risk of severe DKA

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