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      Drugs & Diseases > Endocrinology

      Diabetic Ketoacidosis (DKA) Medication

      Updated: Jan 19, 2021
      • Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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      Medication

      Medication Summary

      Regular and analog human insulins [2] are used for correction of hyperglycemia, unless bovine or pork insulin is the only available insulin. Clinical considerations in treating diabetic ketoacidosis (DKA) include the following:

      • Only short-acting insulin is used for correction of hyperglycemia in DKA.

      • The optimal rate of glucose decline is 100 mg/dL/h.

      • The blood glucose level should not be allowed to fall lower than 200 mg/dL during the first 4-5 hours of treatment.

      • Avoid induction of hypoglycemia because it may develop rapidly during correction of ketoacidosis and may not provide sufficient warning time.

      Treatment of ketoacidosis should aim to correct dehydration, reverse the acidosis and ketosis, reduce plasma glucose concentration to normal, replenish electrolyte and volume losses, and identify the underlying cause.

      According to the 2011 JBDS DKA guideline, patients who are already taking long-acting insulin analogues such as glargine or detemir should be maintained at their usual doses. [25, 26]

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      Rapid-acting insulins

      Class Summary

      Rapid-acting insulins have a rapid onset and short duration of action and are associated with less hypoglycemia than regular insulin.

      Insulin aspart (NovoLog)

      Insulin aspart has an onset of action of 5-15 minutes. The peak effect occurs within 30-90 minutes, and its usual duration of action is 4 hours.

      Insulin glulisine (Apidra)

      Insulin glulisine has an onset of action of 5-15 minutes. The peak effect occurs within 30-90 minutes, and its usual duration of action is 4 hours.

      Insulin lispro (Humalog)

      Insulin lispro has an onset of action of 5-15 minutes, and its usual duration of action is 4 hours.

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      Short-acting insulins

      Class Summary

      Insulin suppresses hepatic glucose output and enhances glucose uptake by peripheral tissues. Insulin also suppresses ketogenesis and lipolysis, stimulates proper use of glucose by the cells, and reduces blood sugar levels. Only short-acting insulin is used for correction of hyperglycemia.

      Regular insulin (Humulin R, Novolin R)

      Regular insulin has an onset of action of 0.5-1 hours. Its peak effect occurs within 2-4 hours, and its usual duration of action is 4-6 hours.

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      Electrolyte Supplement

      Class Summary

      Serum potassium levels initially are high or within the reference range in patients with DKA. This needs to be checked frequently, as values drop very rapidly with treatment. Supplements such as potassium chloride work to correct such electrolyte imbalances.

      Potassium chloride (Klor-Con, K-Dur, Kaon Cl)

      Potassium deficits are high in patients with diabetic ketoacidosis, even with paradoxically high K+ due to acidotic state, which shifts H+ into cells and K+ out of cells into blood. Repletion with potassium phosphate often thought unnecessary, although some recommend giving potassium phosphate to replete both of these electrolytes. Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Monitor the potassium level every 1-2 hours initially.

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      Alkalinizing Agents

      Class Summary

      These agents may be used as a temporizing measure in very severe acidosis and in patients who become hemodynamically unstable because of the acidosis.

      Sodium bicarbonate (Neut)

      Sodium bicarbonate is only infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis. If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary. Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.

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