What are the diagnostic criteria for Diabetic Ketoacidosis (DKA)?

Diagnostic Criteria for Diabetic Ketoacidosis (DKA)

DKA is diagnosed when all three core criteria are present simultaneously: blood glucose >250 mg/dL, venous pH <7.3, serum bicarbonate <15 mEq/L, and elevated blood ketones (preferably β-hydroxybutyrate). 1, 2

Core Diagnostic Triad

All three components must be present for DKA diagnosis:

• Hyperglycemia: Blood glucose >250 mg/dL 1, 2
• Metabolic acidosis: Venous pH <7.3 AND serum bicarbonate <15 mEq/L 1, 2
• Ketosis: Elevated blood β-hydroxybutyrate (β-OHB) or moderate ketonuria/ketonemia 1, 2

Critical caveat: The glucose threshold of >250 mg/dL has been de-emphasized in recent guidelines due to increasing incidence of euglycemic DKA (glucose <250 mg/dL or even <200 mg/dL), particularly in patients on SGLT2 inhibitors, pregnant patients, or those with recent insulin use. 2, 3, 4 Never dismiss DKA because glucose is below 250 mg/dL—the acidosis and ketosis are what define the emergency. 2, 5

Essential Laboratory Workup

Obtain immediately upon presentation:

• Complete metabolic panel: Sodium, potassium, chloride, bicarbonate, BUN, creatinine, glucose 1, 2
• Venous blood gas: pH, pCO2, bicarbonate 1, 2
• Blood β-hydroxybutyrate (β-OHB): This is the gold standard ketone measurement 1, 2, 5
• Anion gap calculation: [Na⁺] - ([Cl⁻] + [HCO₃⁻]), should be >10-12 mEq/L in DKA 1, 2
• Complete blood count with differential, urinalysis, serum osmolality, electrocardiogram 2
• Bacterial cultures (urine, blood, throat) if infection is suspected as a precipitating factor 1

Corrected sodium: Calculate using [measured Na (mEq/L)] + [glucose (mg/dL) - 100]/100 × 1.6 to account for hyperglycemia 1

Severity Classification

DKA severity determines monitoring intensity, prognosis, and treatment location:

Mild DKA

• Venous pH: 7.25-7.30 1, 2
• Bicarbonate: 15-18 mEq/L 1, 2
• Anion gap: >10 mEq/L 2
• Mental status: Alert 1, 2

Moderate DKA

• Venous pH: 7.00-7.24 1, 2
• Bicarbonate: 10-15 mEq/L 1, 2
• Anion gap: >12 mEq/L 2
• Mental status: Drowsy/lethargic 1, 2

Severe DKA

• Venous pH: <7.00 1, 2
• Bicarbonate: <10 mEq/L 1, 2
• Anion gap: >12 mEq/L 2
• Mental status: Stuporous or comatose 1, 2
• Associated with higher morbidity and mortality; often requires ICU admission with central venous and intra-arterial pressure monitoring 1

Critical Ketone Measurement Considerations

Use direct blood β-hydroxybutyrate (β-OHB) measurement, NOT urine ketones or nitroprusside-based tests. 1, 2, 5

The nitroprusside method (used in most urine ketone strips and some serum tests) only measures acetoacetate and acetone, completely missing β-OHB, which is the predominant and strongest ketoacid in DKA. 1, 5 During treatment, β-OHB is converted to acetoacetate, which paradoxically makes nitroprusside tests appear worse even as the patient improves. 1

Optimal β-OHB cut-off values for DKA diagnosis:

• β-hydroxybutyrate: >1.5 mmol/L (manufacturer-suggested) 6 or >6.3 mmol/L (research-derived) 7
• Point-of-care β-OHB testing at triage has 98% sensitivity and 85% specificity for DKA diagnosis 6

Resolution Criteria

DKA is resolved when ALL of the following are met:

• Glucose <200 mg/dL 1, 2
• Venous pH >7.3 1, 2
• Serum bicarbonate ≥18 mEq/L 1, 2
• Anion gap ≤12 mEq/L 1, 2

Important: Ketonemia typically takes longer to clear than hyperglycemia, requiring continued monitoring and insulin therapy even after glucose normalizes. 1, 2 Never discontinue insulin when glucose normalizes—continue until all resolution criteria are met. 1

Monitoring During Treatment

Draw blood every 2-4 hours to measure:

• Electrolytes (sodium, potassium, chloride) 1, 2
• Glucose 1, 2
• Venous pH 1, 2
• β-hydroxybutyrate 1, 2
• Anion gap 1, 2
• BUN, creatinine 1, 2
• Serum osmolality 1, 2

After initial diagnosis, repeat arterial blood gases are generally unnecessary—venous pH and anion gap adequately monitor acidosis resolution, with venous pH typically 0.03 units lower than arterial. 1

Common Diagnostic Pitfalls to Avoid

• Never rely on urine ketones for diagnosis or monitoring, as they miss β-OHB and can be falsely negative early in DKA or falsely positive during treatment 1, 2, 5
• Never dismiss DKA possibility because glucose is <250 mg/dL—euglycemic DKA is increasingly common, especially with SGLT2 inhibitors, pregnancy, recent insulin use, or decreased caloric intake 2, 5, 3, 4
• Never repeat arterial sticks unnecessarily—venous pH suffices for monitoring after initial diagnosis 1
• Never stop insulin when glucose normalizes—ketoacidosis takes longer to resolve than hyperglycemia 1, 2

Differential Diagnosis

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

• Lactic acidosis: Measure blood lactate 2
• Toxic ingestions: Salicylate, methanol, ethylene glycol—identified by specific laboratory tests and clinical presentation 2
• Chronic renal failure 2
• Metformin use (lactic acidosis) 2

Clinical Presentation

Classical presentation includes:

• History: Polyuria, polydipsia, weight loss, vomiting, abdominal pain, weakness, altered mental status 2
• Physical findings: Poor skin turgor, Kussmaul respirations (deep, rapid breathing), tachycardia, hypotension, fruity breath odor (acetone), altered mental status 2
• Up to 25% may have coffee-ground emesis due to hemorrhagic gastritis 2
• Symptoms develop gradually over hours to days 8