Pathophysiology and Presentation

DKA occurs almost exclusively in Type 1 diabetes (though can rarely occur in Type 2 under severe stress) when absolute insulin deficiency forces the body to metabolize fat for energy, producing ketones and metabolic acidosis. Classic findings include blood glucose typically over 250 mg/dL, arterial pH below 7.3, serum bicarbonate under 18 mEq/L, Kussmaul respirations (deep, rapid breathing to blow off CO2 and compensate for acidosis), fruity/acetone breath odor, polyuria, polydipsia, and altered mental status. Serum potassium is often initially elevated or normal despite total body potassium depletion, because acidosis shifts potassium out of cells.

Priority Treatment Sequence

The treatment order is critical: first, IV isotonic fluids (0.9% normal saline) to correct dehydration and dilute glucose; second, IV regular insulin (the only insulin given IV) as a continuous drip to stop ketone production and lower glucose; third, potassium replacement once levels are known and urine output confirmed adequate. Insulin must never be started before potassium is checked because insulin drives potassium into cells, and a patient with normal-appearing potassium can crash into life-threatening hypokalemia within the first hour of insulin therapy, causing dysrhythmias.

Monitoring and Resolution

Monitor blood glucose hourly and electrolytes every 2-4 hours during treatment; glucose should not drop faster than 50-100 mg/dL per hour to prevent cerebral edema, especially in pediatric patients. Once glucose reaches approximately 200-250 mg/dL, IV fluids are switched to dextrose-containing solutions while continuing insulin at a lower rate until the acidosis resolves (anion gap closes), because insulin must continue even as glucose normalizes to fully clear ketones. Transition to subcutaneous insulin only after the patient is eating and ketosis has resolved, overlapping the first subcutaneous dose with the IV drip by 1-2 hours.