Diagnosing Diabetic Ketoacidosis (DKA) - 2024/2025 Guidelines

The Diagnostic Triad

1. Hyperglycemia (or known diabetes)
2. Ketonemia/ketonuria
3. Metabolic acidosis

2024 ADA Consensus Report - Key Updates

1. Glucose Threshold - Revised

2. Ketone Measurement - Beta-Hydroxybutyrate Preferred

• β-OHB ≥3.0 mmol/L = >90% sensitivity and specificity for DKA diagnosis
• Urine ketones (acetoacetate) are no longer first-line because:
  • They underestimate severity early in DKA (β-OHB predominates but is not detected by urine dipstick)
  • They overestimate severity late in DKA (as β-OHB converts to acetoacetate during recovery)

3. Acidosis Criteria

• Venous or arterial pH <7.3
• Serum bicarbonate <18 mmol/L
• Anion gap (Na - Cl - HCO₃) >12 mmol/L - useful but no longer the first-line diagnostic criterion; reserved for resource-limited settings where ketone measurement is unavailable

Note: Venous pH is now preferred over arterial pH - it is approximately 0.03 units lower than arterial pH, avoids arterial puncture risk, and does not change management. - Tintinalli's Emergency Medicine

Severity Classification (ADA 2024)

Essential Initial Workup

• Serum glucose
• Venous blood gas (pH, bicarbonate)
• Serum electrolytes - calculate anion gap; note that measured serum Na is artificially low due to hyperglycemia (correction: add 2.4 mEq/L per 100 mg/dL glucose above 100 mg/dL)
• β-hydroxybutyrate (serum or capillary) - preferred over urine ketones
• Urine ketones - if β-OHB unavailable
• BUN and creatinine - prerenal azotemia is common; creatinine may be falsely elevated if measured by nitroprusside-based assay
• Serum potassium - critical before starting insulin (total body K+ is depleted even when serum K+ appears normal or high due to acidemia-driven extracellular shift)
• CBC - leukocytosis common; WBC >25,000/mm³ or bands >10,000/mm³ suggest infection
• ECG - assess for hyperkalemia/hypokalemia signs; also screen for ischemia as a precipitant
• Serum osmolality - to distinguish from or identify overlap with HHS
• Urinalysis and cultures, CXR - to identify precipitating infection

Differential Diagnosis of Elevated Anion Gap Acidosis

• Alcoholic ketoacidosis
• Starvation ketoacidosis
• Lactic acidosis
• Renal failure
• Toxic ingestions: salicylates, ethylene glycol, methanol

Key Clinical Features at Presentation

• Polyuria, polydipsia, weakness, lethargy
• Nausea, vomiting, abdominal pain (can mimic acute abdomen)
• Kussmaul breathing (deep, rapid respirations - respiratory compensation for acidosis)
• Fruity/acetone breath
• Dehydration signs: dry mucous membranes, tachycardia, orthostatic hypotension
• Altered consciousness in moderate-severe DKA

Resolution Criteria (2024 ADA)

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

Special Considerations

• Euglycemic DKA: Normal or near-normal glucose with confirmed ketonemia and acidosis. Increasingly common with SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin). Do not exclude DKA based on normal glucose alone.
• Hyperchloremic acidosis: Can develop during treatment (from large-volume normal saline), masking true resolution - the anion gap normalizes but bicarbonate remains low. Monitor both anion gap and β-OHB during treatment.
• Overlap with HHS: A mixed picture (ketonemia + hyperosmolality) is not uncommon, especially in type 2 diabetes with intercurrent illness. Manage per DKA protocol if significant ketonemia and acidosis are present.
• Superimposed metabolic alkalosis (from vomiting or diuretics) can mask the true severity - an anion gap disproportionate to the bicarbonate drop should raise this suspicion.