Question

Difficulty: HardPharmacologic Interventions

A 5858-year-old man presents to the emergency department with a 22-day history of nausea, vomiting, abdominal pain, and poor oral intake. He has a history of type 2 diabetes mellitus, hypertension, and hyperlipidemia. His medications include metformin, dapagliflozin, lisinopril, and atorvastatin.

Temperature is 37.1∘37.1^\circ C (98.8∘98.8^\circ F), blood pressure is 102/64102/64 mmHg, pulse is 112112/min, and respirations are 2424/min. Physical examination shows dry mucous membranes and diffuse mild abdominal tenderness without rebound or guarding.

Laboratory studies show:
Na +^+: 132132 mEq/L
K +^+: 4.84.8 mEq/L
Cl −^-: 9898 mEq/L
HCO 3−_3^-: 1414 mEq/L
Urea nitrogen (BUN): 3838 mg/dL
Creatinine: 1.61.6 mg/dL
Glucose: 185185 mg/dL
Ketones: Positive

Arterial blood gas on room air:
pH: 7.247.24
pCO 2_2: 2828 mmHg
pO 2_2: 9595 mmHg

Which of the following intravenous regimens is the most appropriate pharmacologic management for this patient?

  1. A
    5%5\% dextrose and normal saline
  2. B
    Continuous regular insulin and normal saline
  3. Continuous regular insulin, 5%5\% dextrose, and normal salineAnswer
  4. D
    Sodium bicarbonate and normal saline
  5. E
    Subcutaneous insulin aspart and normal saline

Answer

Continuous regular insulin, 5%5\% dextrose, and normal saline
The patient presents with a high anion gap metabolic acidosis, ketonemia, and a relatively normal blood glucose level (185185 mg/dL) in the setting of recent poor oral intake and use of an SGLT2 inhibitor (dapagliflozin). This is classic for euglycemic diabetic ketoacidosis (DKA). SGLT2 inhibitors cause significant urinary glucose loss, lowering serum glucose and subsequently decreasing endogenous insulin secretion while increasing glucagon secretion. This hormonal shift stimulates lipolysis and ketogenesis, leading to DKA without marked hyperglycemia. The cornerstone of DKA management is fluid resuscitation and continuous intravenous regular insulin to halt ketogenesis. However, because the patient's blood glucose is already below the typical 200200-250250 mg/dL threshold, initiating insulin without concurrent dextrose will precipitate severe hypoglycemia. Therefore, the most appropriate pharmacologic regimen must simultaneously include continuous intravenous regular insulin, normal saline for volume expansion, and 5%5\% dextrose to maintain euglycemia while the insulin clears the ketones.

Step-by-Step Solution

1
Calculate the anion gap and identify the primary acid-base disorder.
Anion gap = 132−(98+14)=20132 - (98 + 14) = 20 mEq/L. Combined with pH 7.247.24, this indicates a high anion gap metabolic acidosis.
Determining the acid-base disorder is the first step in diagnosing the cause of the patient's presentation.
2
Correlate the metabolic acidosis with the clinical history and medication list.
The presence of positive ketones, use of dapagliflozin, and blood glucose <250< 250 mg/dL establishes the diagnosis of euglycemic diabetic ketoacidosis (DKA).
SGLT2 inhibitors are a known trigger for euglycemic DKA, particularly during periods of decreased oral intake or acute illness.
3
Select the appropriate fluid and insulin regimen based on the patient's blood glucose level.
Because the blood glucose is 185185 mg/dL (below the typical 200200-250250 mg/dL threshold), the regimen must include dextrose alongside continuous IV insulin and normal saline.
Insulin is required to suppress ketogenesis, but dextrose is necessary to prevent insulin-induced hypoglycemia.

Key Concept

Euglycemic Diabetic Ketoacidosis (DKA) Management
Estimated Time:2m 0s
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