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Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus, most commonly type 1 diabetes, characterized by hyperglycemia, ketosis, and metabolic acidosis. It occurs when insulin deficiency leads to uncontrolled glucose production and lipolysis, resulting in dangerous accumulation of ketone bodies. DKA requires immediate medical intervention and can be triggered by infection, medication non-compliance, or physiological stress.
Insulin deficiency or resistance prevents glucose uptake by cells, leading to compensatory gluconeogenesis and glycogenolysis that causes severe hyperglycemia. Simultaneously, increased lipolysis breaks down fatty acids into ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone), which accumulate faster than they can be metabolized. The resulting ketoacidosis, combined with osmotic diuresis from hyperglycemia, leads to dehydration, electrolyte imbalances, and potentially life-threatening metabolic derangements.
Diagnosis requires the triad of hyperglycemia (>250 mg/dL), ketonemia/ketonuria, and metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L). Clinical presentation includes polyuria, polydipsia, abdominal pain, nausea, vomiting, and altered mental status, with characteristic fruity breath odor from acetone. Treatment involves aggressive fluid resuscitation, insulin therapy, electrolyte replacement (particularly potassium), and identification of precipitating factors, with careful monitoring to prevent complications like cerebral edema.