Diabetic Ketoacidosis Management

Diabetic ketoacidosis (DKA) is defined by the triad of hyperglycemia (>250 mg/dL), ketonemia (beta-hydroxybutyrate >=3 mmol/L or moderate-large urine ketones), and high anion gap metabolic acidosis (pH <7.30, bicarbonate <18 mEq/L). It results from absolute or relative insulin deficiency with counterregulatory hormone excess, leading to lipolysis and ketogenesis.

Common precipitants include new-onset type 1 diabetes, insulin omission, infection, myocardial infarction, pancreatitis, glucocorticoids, atypical antipsychotics, and SGLT2 inhibitors (euglycemic DKA). Patients present with polyuria, polydipsia, abdominal pain, vomiting, Kussmaul respirations, fruity breath, and altered mental status in severe cases.

Management follows ADA/JBDS algorithms: aggressive isotonic crystalloid (1-1.5 L NS in first hour, then 250-500 mL/h adjusted to corrected sodium), fixed-rate IV insulin infusion (0.1 U/kg/h after potassium >3.3), potassium replacement when serum K+ <5.3, dextrose addition at glucose <200-250, and bicarbonate only for pH <6.9. Monitor for cerebral edema in pediatric DKA. Transition to subcutaneous basal-bolus insulin once anion gap closes. Diabetes education and follow-up endocrinology essential to prevent recurrence.