A 30-year-old man with type 1 diabetes mellitus (DM) presents to the emergency department (ED). His blood pressure (BP) is 100/70 mm Hg and heart rate (HR) is 140 beats/minute. His blood glucose is 750 mg/dL, potassium level is 2.9 mEq/L, bicarbonate is 5 mEq/L, and arterial pH is 7.1. His urine is positive for ketones. Which of the following is the best initial therapy for this patient?
a. Administer a 2 L normal saline (NS) bolus and 20 units of subcutaneous (SQ) insulin
b. Administer 2 ampules of intravenous (IV) sodium bicarbonate and 10 units of IV insulin
c. Administer a 2 L NS bolus and 40 mEq IV potassium chloride
d. Administer a 2 L NS bolus followed by an insulin drip at 0.1 units/kg/hour
e. Administer 5 mg IV metoprolol and 2L NS bolus
The answer is c. While the mainstay of treatment for DKA is aggressive IV fluid resuscitation and IV insulin therapy, this patient’s serum potassium level is markedly low. He requires fluid resuscitation and potassium correction. If the initial serum potassium is below 3.3 mEq/L, IV KCl should be given prior to administration of insulin. Failure to correct hypokalemia prior to insulin administration could cause respiratory muscle weakness, cardiac arrhythmias, or even cardiac arrest due to intracellular movement of potassium. Once the serum potassium is between 3.3 and 5.3 mEq/L, insulin infusion at 0.1 units/kg/hour is indicated along with IV KCl (20-30 mEq) is added to each liter of IV replacement fluid and continued until the serum potassium concentration has increased to the normal range of 4 to 5 mEq/L.
In DKA, the average adult has a water deficit of 5 to 10 L. After the first 2 L of fluid, (d) regular insulin is administered at a rate of 0.1 units/kg/hour. Insulin must be administered for ketosis and acidosis to resolve. There is no consensus on need for an insulin bolus prior to starting an infusion. Such a bolus may negatively affect the already total body deficit of potassium and in recent years has fallen out of favor in the initial treatment of DKA. Intramuscular and SQ insulin administration (a) is avoided in DKA as absorption may be erratic secondary to volume depletion and poor perfusion. Currently, no study shows a benefit of using bicarbonate in DKA (b). Bicarbonate administration can cause worsening hypokalemia, paradoxical central nervous system (CNS) acidosis, impaired oxyhemoglobin dissociation, hypertonicity, and sodium overload. Metoprolol (e), a β-blocker, is not indicated in DKA. The tachycardia in DKA is secondary to volume depletion and acidosis. Correcting the underlying cause will treat the tachycardia.