Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergent condition that often manifests in the diabetic patient with leukocytosis and an acute surgical abdominal emergency or with nausea, vomiting, lethargy, and signs of hypovolemia. The priorities are to restore intravascular volume (usually rapid intravenous administration of 1 L of saline); administer regular insulin (0.2 unit/kg) followed by an infusion at a rate of 0.1 unit/kg/hour; eliminate the ketonemia; control blood glucose; and correct the underlying problem (e.g., antibiotics for urosepsis or pneumonia). Patients with ketoacidosis are dehydrated as a result of glucosuria; because the dehydration is caused by water and electrolyte loss, colloids are not indicated. If the patient's osmolality is elevated, 0.45% sodium chloride can be administered, and the volume administered should be guided by the hemodynamic response and urinary output. When the blood glucose falls below 250 mg/dL, dextrose should be added to the fluids. Urine or blood ketones are monitored every 2 hours after the blood glucose is within 100 to 200 mg/dL. If ketones are still present, the rates of glucose and insulin infusions should both be increased.

Osmotic diuresis promotes loss of sodium, potassium, magnesium, and phosphate. Despite total-body deficiencies, however, their concentrations may be elevated at the time of presentation because of severe water loss. The best treatment for hyperkalemia in these patients is appropriate therapy for the diabetic ketoacidosis. Potassium levels decrease rapidly with appropriate volume replacement and insulin therapy. Most patients require electrolyte replacement after volume expansion has begun. Alternatively, severe hyperglycemia may extract water from the intracellular space and may dilute the electrolyte concentrations. If the initial potassium level is elevated or the patient is anuric, potassium should not be administered. As hydration improves and urinary output increases, potassium, magnesium, and phosphorus should be administered and levels monitored frequently. In general, acidosis should not be treated with buffers. The ketoacidosis is corrected as insulin and glucose levels improve, and the lactic acidosis resulting from poor perfusion responds to intravascular fluid replacement. If the pH approaches 7.15, the bicarbonate ion concentration is less than 10 mEq/L and hypotension fails to respond to intravascular fluid administration, sodium bicarbonate therapy may be required.