Diabetic Ketoacidosis — DKA

DKA occurs when absolute or relative insulin deficiency forces the body to break down fat for energy, producing ketone bodies (beta-hydroxybutyrate, acetoacetate, acetone) that overwhelm buffering capacity and cause metabolic acidosis. Classic lab findings: blood glucose typically 250–600 mg/dL, arterial pH below 7.30, serum bicarbonate below 18 mEq/L, positive serum ketones, and an elevated anion gap. Clinical presentation includes Kussmaul respirations (deep, rapid breathing — the lungs compensating for acidosis), fruity acetone breath, polyuria, polydipsia, nausea/vomiting, abdominal pain, and altered mental status. Treatment priorities follow a specific sequence: aggressive IV fluid resuscitation first (0.9% NS initially to correct dehydration), then continuous IV regular insulin infusion (not subcutaneous, not rapid-acting analogs), and potassium replacement guided by serum levels — potassium must be at least 3.3 mEq/L before starting insulin, because insulin drives potassium intracellularly and can cause fatal hypokalemia. Monitor glucose hourly; when it drops to 250 mg/dL, switch IV fluids to D5 with half-normal saline to prevent hypoglycemia and cerebral edema while continuing the insulin drip until the anion gap closes.