What is the primary concern and management for a type 2 diabetic patient with elevated beta-hydroxybutyrate (BHB) and an increased anion gap?

Diabetic Ketoacidosis (DKA) in Type 2 Diabetes

This patient has diabetic ketoacidosis (DKA) and requires immediate hospitalization for intravenous insulin therapy, aggressive fluid resuscitation, and electrolyte monitoring—regardless of the blood glucose level. 1, 2

Diagnostic Confirmation

Your patient meets diagnostic criteria for DKA based on:

• Elevated beta-hydroxybutyrate (the predominant and preferred ketone marker) 1, 2
• Anion gap of 19 mEq/L (elevated, as normal is ≤10-12 mEq/L) 1, 2
• Presumed metabolic acidosis (pH <7.3 and/or bicarbonate <18 mEq/L should be confirmed) 1, 2

Critical point: This could be euglycemic DKA if glucose is <250 mg/dL, which is increasingly common in type 2 diabetes, particularly with SGLT2 inhibitor use, reduced oral intake, or alcohol use. 1, 2, 3 The presence of elevated ketones and anion gap makes this DKA regardless of glucose level. 1

Immediate Management Algorithm

Step 1: Confirm Severity and Admit

• Obtain venous blood gas immediately for pH and bicarbonate 1
• Complete metabolic panel with calculated anion gap 1, 2
• Direct beta-hydroxybutyrate measurement (not urine ketones, which are unreliable) 1, 2
• Admit to hospital for all patients with confirmed DKA; severe cases (pH <7.0) require ICU-level monitoring 4

Step 2: Initiate Insulin Therapy

For euglycemic DKA (glucose <250 mg/dL):

• Start continuous IV regular insulin at 0.1 units/kg/hour 1
• Add dextrose 5% to IV fluids from the start to prevent severe hypoglycemia 1
• Target glucose 150-200 mg/dL during treatment 1
• Continue insulin infusion despite euglycemia until ketoacidosis resolves 1

For traditional DKA (glucose ≥250 mg/dL):

• Start continuous IV regular insulin at 0.1 units/kg/hour 4
• Add dextrose to fluids once glucose falls to <250 mg/dL 4

Step 3: Fluid and Electrolyte Management

• Aggressive IV fluid resuscitation with isotonic saline 4, 2
• Potassium replacement is critical: Add 20-30 mEq potassium (2/3 KCl, 1/3 KPO4) per liter once serum K+ <5.5 mEq/L 4
• Delay insulin if potassium <3.3 mEq/L to prevent life-threatening arrhythmias 4, 1
• Monitor electrolytes every 2-4 hours 4

Step 4: Monitor for Resolution

DKA is resolved when ALL of the following are met: 1, 2

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

Step 5: Transition to Subcutaneous Insulin

• Administer basal insulin (glargine or detemir) 2-4 hours before stopping IV insulin to prevent rebound ketoacidosis 1
• Start multiple-dose subcutaneous regimen once patient can eat 1
• For type 2 diabetes patients, some may eventually transition to oral agents after stabilization 4

Critical Pitfalls to Avoid

Do not rely on urine ketones: Nitroprusside-based tests do not measure beta-hydroxybutyrate and should not guide treatment decisions. 4, 1, 2

Do not stop insulin when glucose normalizes: In euglycemic DKA, insulin must continue until acidosis resolves, not just until glucose is controlled. 1

Do not overlook potassium: Despite initial hyperkalemia, total body potassium is depleted, and levels will drop precipitously with insulin therapy. 4

Do not assume type 2 diabetes excludes DKA: While less common than in type 1, DKA occurs in type 2 diabetes, especially with precipitating factors like infection, medication non-adherence, or SGLT2 inhibitor use. 2, 3, 5

Identify Precipitating Factors

Common triggers requiring treatment: 2, 3

• Infection (most common)
• Insulin omission or inadequate dosing
• Myocardial infarction or stroke
• SGLT2 inhibitor use
• Alcohol abuse
• New medications (corticosteroids, thiazides)

Special consideration: If the patient is on an SGLT2 inhibitor (canagliflozin, empagliflozin, dapagliflozin), this significantly increases euglycemic DKA risk and should be discontinued. 2, 6, 3