What is the appropriate management for a patient with hyperglycemia, elevated beta-hydroxybutyrate, and metabolic derangements suggestive of diabetic ketoacidosis?

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Management of Euglycemic Diabetic Ketoacidosis

This patient does NOT have diabetic ketoacidosis despite the elevated beta-hydroxybutyrate, because the pH is normal (7.43) and bicarbonate is normal (28 mEq/L), which are incompatible with DKA diagnosis. 1, 2, 3

Why This Is Not DKA

  • DKA requires arterial pH <7.30, serum bicarbonate <18 mEq/L, and positive ketones - this patient has pH 7.43 and bicarbonate 28 mEq/L, both completely normal 1, 2, 3

  • The diagnostic criteria from the American Diabetes Association mandate blood glucose >250 mg/dL (present at 500 mg/dL), arterial pH <7.30 (absent - patient has 7.43), serum bicarbonate <18 mEq/L (absent - patient has 28 mEq/L), and presence of ketonemia 1, 2, 3

  • While beta-hydroxybutyrate of 10 mmol/L is markedly elevated (normal <0.5 mmol/L), ketosis without acidosis does not constitute ketoacidosis 4, 5

Appropriate Management Approach

Immediate Assessment

  • Verify the laboratory values - confirm pH, bicarbonate, and beta-hydroxybutyrate measurements are accurate, as this constellation (severe ketosis with normal acid-base status) is unusual 1, 2

  • Check anion gap - calculate anion gap to assess for any metabolic acidosis that might be masked by a concurrent metabolic alkalosis 1, 2, 3

  • Assess for SGLT2 inhibitor use - euglycemic DKA can occur with SGLT2 inhibitors, though this patient's glucose of 500 mg/dL argues against true euglycemic DKA 1, 2

Treatment Strategy

  • Administer insulin therapy to address hyperglycemia (blood glucose 500 mg/dL) and suppress ongoing ketogenesis, even though acidosis is absent 1, 2, 3

  • Provide intravenous fluids with isotonic saline to restore volume and improve tissue perfusion, which will help clear ketones 1, 2, 3

  • Monitor closely for development of acidosis - check venous pH and bicarbonate every 2-4 hours, as the patient could progress to true DKA if insulin deficiency worsens 1, 2, 3

  • Continue insulin until beta-hydroxybutyrate normalizes (<1.5 mmol/L indicates resolution of ketosis), even after glucose is controlled 5

Key Monitoring Parameters

  • Blood glucose every 1-2 hours during active treatment 2, 3

  • Venous pH, bicarbonate, and anion gap every 2-4 hours to detect any progression to true DKA 1, 2, 3

  • Beta-hydroxybutyrate levels correlate better with ketosis resolution than urine ketones, which can remain positive even after blood ketones normalize 4, 6, 5

  • Serum potassium every 2-4 hours as insulin therapy drives potassium intracellularly and can cause life-threatening hypokalemia 1, 2, 3, 7

Critical Pitfall to Avoid

  • Do not treat this as full DKA with aggressive bicarbonate administration - bicarbonate is not indicated when pH >7.0, and this patient's pH is normal at 7.43 1, 2, 3

  • Do not delay insulin therapy waiting for acidosis to develop - the elevated beta-hydroxybutyrate and hyperglycemia require insulin treatment regardless of pH status 1, 2

  • Do not stop insulin when glucose reaches 250 mg/dL - add dextrose to IV fluids and continue insulin at reduced rate until beta-hydroxybutyrate normalizes to ensure complete ketosis resolution 1, 2, 3

References

Guideline

Assessment and Management of Diabetic Ketoacidosis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Management of Diabetic Ketoacidosis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Management of Diabetic Ketoacidosis (DKA)

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

[Capillary beta-hydroxybutyrate determination for monitoring diabetic ketoacidosis].

Endocrinologia y nutricion : organo de la Sociedad Espanola de Endocrinologia y Nutricion, 2011

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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