Yes, DKA Can Occur with a Blood Glucose of 135 mg/dL
Yes, diabetic ketoacidosis can absolutely occur with a blood glucose level of 135 mg/dL—this is called euglycemic DKA, and the diagnosis depends on metabolic acidosis and ketosis, not just hyperglycemia. 1, 2
Understanding Euglycemic DKA
The most recent American Diabetes Association guidelines explicitly recognize that DKA presentation has "considerable variability, ranging from euglycemia or mild hyperglycemia and acidosis to severe hyperglycemia." 1 This represents a critical shift from older diagnostic criteria.
Classic vs. Euglycemic DKA Diagnostic Criteria
Classic DKA requires all three of the following 1, 2, 3:
- Blood glucose >250 mg/dL
- Arterial pH <7.3 AND serum bicarbonate <18 mEq/L (or <15 mEq/L by some criteria)
- Positive ketones (moderate ketonuria or ketonemia)
Euglycemic DKA is diagnosed when 2, 4, 5:
- Blood glucose <200-250 mg/dL (can be as low as normal range)
- Metabolic acidosis: pH <7.3 AND bicarbonate <18 mEq/L
- Elevated β-hydroxybutyrate (βOHB) in blood
- Elevated anion gap
Critical Diagnostic Approach for Your Patient
Essential Laboratory Tests to Order Immediately
When you suspect DKA with a glucose of 135 mg/dL, you must obtain 2, 3:
- Arterial or venous blood gas (venous pH is typically 0.03 units lower than arterial and is acceptable) 1
- Serum β-hydroxybutyrate (βOHB) - this is the preferred test, NOT urine ketones 2, 3
- Basic metabolic panel with calculated anion gap
- Serum bicarbonate level
Why β-Hydroxybutyrate Matters
Do NOT rely on urine ketone dipsticks or nitroprusside-based tests alone. 2, 3 These only detect acetoacetate and acetone, NOT β-hydroxybutyrate, which is the predominant ketone in DKA. 2 During treatment, βOHB converts to acetoacetate, which can falsely suggest worsening ketosis when the patient is actually improving. 1, 2
Common Causes of Euglycemic DKA
SGLT2 Inhibitors (Most Important Modern Cause)
SGLT2 inhibitors significantly increase DKA risk and commonly cause euglycemic DKA. 2 If your patient is on empagliflozin, dapagliflozin, canagliflozin, or ertugliflozin, this is your most likely culprit.
Other Precipitating Factors 4, 5:
- Starvation or decreased caloric intake (nausea, vomiting, fasting)
- Insulin pump failure or recent insulin use prior to presentation
- Pregnancy
- Heavy alcohol use
- Cocaine abuse
- Acute illness (infection, pancreatitis, sepsis)
- Chronic liver disease
Treatment Approach for Euglycemic DKA
Critical Management Principle
Continue insulin therapy despite normal glucose levels. 3 This is the most common pitfall—clinicians stop insulin when glucose normalizes, but the ketoacidosis persists.
Specific Treatment Protocol 3, 5:
- Start IV insulin infusion as you would for classic DKA
- Add dextrose (10% or 20%) to IV fluids while continuing insulin infusion 3, 5
- Aggressive IV fluid resuscitation 1, 5
- Monitor for resolution based on:
- pH >7.3
- Bicarbonate ≥18 mEq/L
- Anion gap ≤12 mEq/L
- NOT glucose levels 3
Do NOT Stop Insulin When Glucose Normalizes
The most dangerous error is interrupting insulin therapy when glucose normalizes before ketoacidosis resolves. 3 You must continue insulin to suppress ketogenesis and clear ketones, while providing adequate dextrose to prevent hypoglycemia.
Differential Diagnosis to Consider
Alcoholic Ketoacidosis (AKA)
AKA can present with glucose levels from normal to mildly elevated (rarely >250 mg/dL) or even hypoglycemia. 1, 2 Distinguish by:
- Clinical history of alcohol use
- Typically less severe acidosis than DKA
- May have concurrent hypoglycemia
Starvation Ketosis
Starvation ketosis typically has 1:
- Serum bicarbonate usually not lower than 18 mEq/L
- Less severe acidosis than DKA
- Clinical history of prolonged fasting