MKSAP quiz: Diabetic ketoacidosis

This month's quiz asks readers to choose a treatment for a patient with type 1 diabetes who uses an insulin pump and is being evaluated for diabetic ketoacidosis.

A 21-year-old woman with type 1 diabetes mellitus is evaluated in the emergency department for diabetic ketoacidosis. She uses an insulin pump.

On physical examination, blood pressure is 100/60 mm Hg, pulse rate is 110/min, respiration rate is 20/min, and oxygen saturation is 98% with the patient breathing ambient air. Her mucous membranes are dry, and she has mild abdominal discomfort to palpation. Other than tachycardia, the remainder of the physical examination is normal.

Laboratory studies show potassium 3.2 mEq/L (3.2 mmol/L), sodium 138 mEq/L (138 mmol/L), bicarbonate 10 mEq/L (10 mmol/L), phosphorus 3 mg/dL (0.97 mmol/L), glucose 500 mg/dL (27.8 mmol/L), and anion gap 22 mEq/L (22 mmol/L). β-Hydroxybutyrate is elevated and venous pH is 7.2.

Fluid resuscitation with 0.9% saline is initiated.

Which of the following is the most appropriate intravenous treatment?

A. Insulin
B. Phosphorus
C. Potassium chloride
D. Sodium bicarbonate

Reveal the Answer

MKSAP Answer and Critique

The correct answer is C. Potassium chloride. This item is available to MKSAP 19 subscribers as item 72 in the Endocrinology and Metabolism section. More information about MKSAP is online.

The most appropriate next step is to administer potassium chloride (Option C), 20 to 30 mEq/L (20-30 mmol/L), until the potassium level is greater than 3.3 mEq/L (3.3 mmol/L); then 20 to 30 mEq/L (20-30 mmol/L) of potassium can be added to each liter of saline thereafter. Glucosuria in diabetic ketoacidosis (DKA) causes an osmotic diuresis and severe volume depletion, which may progress to lethargy, obtundation, and death if the hyperglycemia, dehydration, and electrolyte abnormalities are not treated aggressively and early. Aggressive intravenous volume replacement with 0.9% saline is indicated. Electrolyte deficits, such as potassium, should be replaced, and hyperglycemia should be corrected with intravenous insulin. In DKA, total body potassium levels are depleted because of shifts from the intracellular to extracellular space caused by the ketoacidosis and insufficient insulin. Potassium urinary losses are generated by the glucose osmotic diuresis and result in potassium depletion. Normal or low serum potassium levels indicate a depletion of body stores and require supplementation before insulin therapy is initiated.

Initiating insulin (Option A) before potassium replacement could cause life-threatening hypokalemia because insulin shifts potassium into the intracellular space. Therefore, potassium should be replaced to above 3.3 mEq/L (3.3 mmol/L) before initiating insulin.

Because DKA is often associated with hypophosphatemia, phosphorus levels (Option B) should be monitored. However, routine replacement of phosphorus is not indicated because no therapeutic benefit is evident, except in severe hypophosphatemia (<1 mg/dL [0.32 mmol/L]). Adverse effects include hypocalcemia and hypomagnesemia. Following correction of DKA, hypophosphatemia can generally be treated with food rich in phosphorus, such as dairy products.

Sodium bicarbonate (Option D) is only considered in patients with severe acidosis (pH <6.9). Alkali therapy may prolong the recovery from DKA and may result in a residual metabolic alkalosis once DKA is resolved.

Key Points

  • In diabetic ketoacidosis, potassium should be replaced to greater than 3.3 mEq/L (3.3 mmol/L) before initiating insulin.
  • Initiating insulin before potassium replacement will worsen hypokalemia because insulin shifts potassium into the intracellular space and may result in life-threatening hypokalemia.