What are the criteria for diabetic ketoacidosis?

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Diagnostic Criteria for Diabetic Ketoacidosis

Diabetic ketoacidosis is diagnosed when all three of the following criteria are simultaneously present: blood glucose >250 mg/dL, arterial pH <7.30, serum bicarbonate <15 mEq/L, and the presence of ketones in serum or urine. 1, 2

Core Biochemical Triad

The American Diabetes Association requires all three components for DKA diagnosis 1, 2:

  • Hyperglycemia: Blood glucose >250 mg/dL 1, 2
  • Metabolic acidosis: Arterial pH <7.30 AND serum bicarbonate <15-18 mEq/L 1, 2
  • Ketosis: Positive serum or urine ketones 1, 2

The anion gap should be >10 mEq/L, calculated as: (Na+) - (Cl- + HCO3-) 1, 2

Severity Stratification

DKA severity is classified based on the degree of acidosis and mental status 2:

  • Mild DKA: pH 7.25-7.30, bicarbonate 15-18 mEq/L, anion gap >10 mEq/L, patient alert 2
  • Moderate DKA: pH 7.00-7.24, bicarbonate 10 to <15 mEq/L, anion gap >12 mEq/L, patient alert or drowsy 2
  • Severe DKA: pH <7.00, bicarbonate <10 mEq/L, anion gap >12 mEq/L, patient stuporous or comatose 2

Critical Ketone Measurement Considerations

Blood β-hydroxybutyrate (β-OHB) measurement is the preferred method for diagnosing and monitoring DKA, not nitroprusside-based urine or serum tests. 2

This distinction is clinically crucial because 2:

  • Nitroprusside methods (urine dipsticks, serum tablets) only detect acetoacetate and acetone, NOT β-OHB
  • β-OHB is the predominant ketone body in DKA
  • During treatment, β-OHB converts to acetoacetate, making nitroprusside tests falsely suggest worsening ketosis when the patient is actually improving

Euglycemic DKA Exception

A critical caveat: hyperglycemia has been de-emphasized in recent guidelines due to increasing incidence of euglycemic DKA, particularly with SGLT2 inhibitor use. 2, 3

Euglycemic DKA is diagnosed when 2, 4:

  • Blood glucose <250 mg/dL (sometimes <200 mg/dL)
  • Metabolic acidosis still present (pH <7.3, bicarbonate <18 mEq/L)
  • Elevated β-OHB or positive ketones

SGLT2 inhibitors significantly increase DKA risk and commonly cause euglycemic DKA 2. Other causes include recent insulin use, decreased caloric intake, heavy alcohol consumption, chronic liver disease, and pregnancy 4.

Essential Initial Laboratory Workup

When DKA is suspected, obtain 2:

  • Plasma glucose
  • Arterial blood gas (pH, bicarbonate) or venous pH (acceptable alternative, typically 0.03 units lower than arterial) 5
  • Serum electrolytes with calculated anion gap
  • Blood urea nitrogen and creatinine
  • Serum β-OHB (preferred) or serum/urine ketones
  • Serum osmolality
  • Complete blood count with differential
  • Urinalysis
  • Electrocardiogram

Resolution Criteria

DKA is considered resolved when all of the following are achieved 1, 2:

  • Blood glucose <200 mg/dL
  • Serum bicarbonate ≥18 mEq/L
  • Venous pH >7.3

Differential Diagnosis Pitfalls

DKA must be distinguished from other causes of high anion gap metabolic acidosis 2:

  • Alcoholic ketoacidosis: History of alcohol use, glucose typically normal to mildly elevated (rarely >250 mg/dL) or hypoglycemic 2
  • Starvation ketosis: Less severe acidosis and lower ketone levels 2
  • Lactic acidosis: Elevated lactate levels
  • Toxic ingestions: Methanol, ethylene glycol, salicylates

References

Guideline

Diagnostic and Management of Diabetic Ketoacidosis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Diagnostic Criteria and Management of Diabetic Ketoacidosis (DKA)

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Diabetic Ketoacidosis: Evaluation and Treatment.

American family physician, 2024

Research

Euglycemic Diabetic Ketoacidosis: A Review.

Current diabetes reviews, 2017

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

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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