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Difficulty: HardPhysiological Adaptation

A client is admitted to the intensive care unit with severe diabetic ketoacidosis (DKA). The client is lethargic with a blood glucose of 680 mg/dL (37.7 mmol/L), a serum pH of 7.12, and a blood pressure of 82/48 mm Hg. Arrange the following collaborative nursing actions in the priority order they should be implemented.

  1. 1Establish peripheral access and administer a rapid bolus of 0.9% sodium chloride.
  2. 2Evaluate the initial comprehensive metabolic panel to ensure the serum potassium is at least 3.3 mEq/L (3.3 mmol/L).
  3. 3Initiate a continuous intravenous infusion of regular insulin at 0.1 units/kg/hr.
  4. 4Incorporate 5% dextrose into the intravenous hydration fluids once the blood glucose reaches 250 mg/dL (13.9 mmol/L).

Answer

The correct sequence is: 1. Administer a rapid bolus of 0.9% sodium chloride to restore volume; 2. Evaluate the serum potassium level to ensure safety; 3. Initiate a continuous intravenous infusion of regular insulin to correct acidosis; 4. Incorporate 5% dextrose into the hydration fluids once glucose reaches 250 mg/dL to prevent hypoglycemia.
In the management of severe diabetic ketoacidosis (DKA), the immediate physiological priority is to address life-threatening hypovolemia and impaired tissue perfusion caused by osmotic diuresis; therefore, isotonic fluid resuscitation is the first step. Following the initiation of fluids, the nurse must verify the serum potassium level. Insulin therapy causes an intracellular shift of potassium, which can precipitate fatal cardiac arrhythmias if the client is already hypokalemic. Once a safe potassium level is confirmed (greater than 3.3 mEq/L), a continuous regular insulin infusion is started to halt ketone production and correct the acidosis. Finally, as the blood glucose decreases to approximately 250 mg/dL (13.9 mmol/L), dextrose must be added to the intravenous fluids to prevent hypoglycemia and to avoid rapid osmotic shifts that can lead to cerebral edema.

Step-by-Step Solution

1
Administer a rapid bolus of 0.9% sodium chloride.
Intravascular volume is restored, and tissue perfusion improves.
Severe osmotic diuresis in DKA leads to profound dehydration and hypovolemic shock (evidenced by the blood pressure of 82/48 mm Hg), which must be addressed immediately.
2
Evaluate the initial comprehensive metabolic panel for the serum potassium level.
Ensures the serum potassium is at least 3.3 mEq/L (3.3 mmol/L).
Insulin therapy drives potassium into the intracellular space. Administering insulin without confirming adequate potassium levels can trigger fatal arrhythmias.
3
Initiate a continuous intravenous infusion of regular insulin.
Ketone production is halted, and metabolic acidosis is corrected.
Once perfusion is improving and potassium is safe, regular insulin is required to reverse the underlying metabolic derangements of DKA.
4
Incorporate 5% dextrose into the intravenous hydration fluids.
Blood glucose slowly stabilizes without dropping too rapidly.
When blood glucose reaches 250 mg/dL (13.9 mmol/L), adding dextrose prevents iatrogenic hypoglycemia and protects against rapid osmotic changes that cause cerebral edema.

Key Concept

The physiological priority in Diabetic Ketoacidosis (DKA) is sequential management: fluid volume restoration, electrolyte verification, insulin administration, and hypoglycemia prevention.
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Physiological Adaptation

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