Soru

Zorluk: ZorEndocrinology and Metabolism

A 22-year-old man with a history of type 1 diabetes mellitus is brought to the emergency department due to progressive lethargy, nausea, vomiting, and diffuse abdominal pain over the past 24 hours. He reports having a severe sore throat and fever for the last three days. His temperature is 37.5°C (99.5°F), blood pressure is 92/58 mm Hg, pulse is 128/min, and respirations are 28/min and deep. Physical examination reveals dry mucous membranes, delayed capillary refill, and a fruity breath odor. Laboratory evaluation reveals:

Laboratory TestResult
Serum glucose580 mg/dL
Serum sodium132 mEq/L
Serum potassium3.1 mEq/L
Serum chloride98 mEq/L
Serum bicarbonate10 mEq/L
Blood urea nitrogen35 mg/dL
Serum creatinine1.6 mg/dL
Arterial pH7.15
UrinalysisLarge ketones, large glucose

Arrange the following management steps in the most appropriate chronological sequence for this patient.

  1. 1Administer intravenous 0.9% sodium chloride bolus
  2. 2Administer intravenous potassium chloride
  3. 3Initiate continuous intravenous regular insulin infusion
  4. 4Add 5% dextrose to the intravenous fluids
  5. 5Administer subcutaneous long-acting insulin

Cevap

The correct sequence is: Intravenous 0.9% sodium chloride bolus → Intravenous potassium chloride → Continuous intravenous regular insulin infusion → Add 5% dextrose to intravenous fluids → Subcutaneous long-acting insulin.
The correct sequence prioritizes immediate life-saving interventions while preventing iatrogenic complications. Intravenous fluids (0.9% NaCl) are universally the first step in DKA to restore volume and renal perfusion. Next, because the patient's potassium is critically low (< 3.3 mEq/L), potassium chloride must be given before insulin to prevent life-threatening hypokalemia. Once potassium is confirmed to be ≥ 3.3 mEq/L, an intravenous insulin infusion is started to halt ketogenesis. As glucose levels fall below 250 mg/dL, dextrose is added to the fluids to prevent hypoglycemia while allowing continued insulin administration to close the anion gap. Finally, once the anion gap resolves and the patient can eat, they are transitioned to subcutaneous insulin.

Adım Adım Çözüm

1
Assess volume status and initiate fluid resuscitation.
Intravenous 0.9% normal saline is given immediately.
The patient is hypotensive, tachycardic, and severely dehydrated due to osmotic diuresis; volume expansion is always the first priority.
2
Evaluate initial serum potassium level before administering insulin.
Intravenous potassium chloride is administered next.
The patient's potassium is 3.1 mEq/L (below the critical 3.3 mEq/L threshold). Insulin causes an intracellular shift of potassium, so giving insulin now would cause life-threatening hypokalemia.
3
Initiate insulin therapy once potassium is safe.
Continuous intravenous regular insulin infusion is started.
Insulin is required to stop ketogenesis and close the anion gap. It is safe to start only after potassium is ≥ 3.3 mEq/L.
4
Monitor glucose and adjust intravenous fluids.
Dextrose 5% is added to the intravenous fluids.
When serum glucose reaches 200-250 mg/dL, dextrose must be added to prevent hypoglycemia while the insulin infusion continues to clear ketones.
5
Transition to maintenance diabetes therapy.
Subcutaneous long-acting insulin is administered.
This is done when the anion gap is closed (usually ≤ 12 mEq/L) and the patient can eat, allowing for the eventual discontinuation of the IV insulin drip (1-2 hours later).

Anahtar Kavram

In the management of diabetic ketoacidosis, if the initial serum potassium is < 3.3 mEq/L, potassium repletion must precede insulin therapy to prevent severe, potentially fatal insulin-induced hypokalemia.
Bu soruyu puanla