How to manage diabetic ketoacidosis (DKA) in an adult patient with diabetes and hyperglycemia, possibly with ketonuria, when serum bicarbonate levels are not available, but serum electrolytes, glucose, Blood Urea Nitrogen (BUN), and urinalysis results are available?

Managing DKA Without Serum Bicarbonate: Use Anion Gap and Clinical Criteria

When serum bicarbonate is unavailable, diagnose and manage DKA using the anion gap (>10-12 mEq/L), arterial or venous pH (<7.3), hyperglycemia (typically >250 mg/dL, though euglycemic variants exist), and presence of ketones in blood or urine. 1, 2

Diagnostic Approach Without Bicarbonate

Calculate the Anion Gap

• Use the formula: Anion Gap = [Na+] - ([Cl-] + [CO2/HCO3-]) 1
• If CO2/bicarbonate is truly unavailable, calculate using: Anion Gap = [Na+] - [Cl-] - 24 (assuming normal bicarbonate of 24 mEq/L as baseline) 1
• An anion gap >10 mEq/L indicates mild DKA; >12 mEq/L indicates moderate to severe DKA 1
• The anion gap directly correlates with ketoacid accumulation and DKA severity 1

Obtain Arterial or Venous Blood Gas

• Arterial pH <7.3 confirms metabolic acidosis and is a diagnostic criterion for DKA 3, 2
• Venous pH can substitute for arterial pH (typically 0.03 units lower than arterial) and is less invasive 3
• Do not rely on urine ketones alone—they are insufficient for diagnosis and monitoring 4

Measure Ketones Appropriately

• Measure serum beta-hydroxybutyrate directly if available—this is the preferred method 3, 2
• Avoid nitroprusside-based tests (urine or serum) for monitoring treatment response, as they only detect acetoacetate and acetone, not beta-hydroxybutyrate 3, 2
• During treatment, beta-hydroxybutyrate converts to acetoacetate, which may falsely suggest worsening ketosis with nitroprusside testing 3, 2

Initial Management Protocol

Fluid Resuscitation (First Priority)

• Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour (1-1.5 liters in average adults) 3, 4
• After the first hour, adjust based on corrected serum sodium 3:
  • Use 0.45% NaCl at 4-14 mL/kg/hour if corrected sodium is normal or elevated 3
  • Continue 0.9% NaCl at similar rate if corrected sodium is low 3
• Correct serum sodium for hyperglycemia: add 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL 3, 4
• Target correction of fluid deficits within 24 hours, with osmolality change not exceeding 3 mOsm/kg H2O per hour 3, 4

Insulin Therapy

• First, exclude hypokalemia (K+ <3.3 mEq/L) before starting insulin 3, 5
• For moderate-severe DKA: Give IV bolus of regular insulin 0.15 units/kg, followed by continuous infusion at 0.1 units/kg/hour 3
• For mild DKA: Can use subcutaneous or intramuscular regular insulin 0.4-0.6 units/kg (half IV bolus, half SC/IM), then 0.1 units/kg SC/IM hourly 3
• Target glucose decline of 50-75 mg/dL per hour 3
• If glucose doesn't fall by 50 mg/dL in first hour, check hydration status and double insulin infusion hourly until target decline achieved 3
• When glucose reaches 250 mg/dL, add 5% dextrose to IV fluids and continue insulin 3, 6

Potassium Replacement (Critical)

• Once renal function is confirmed and serum potassium is known, add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO4) 3, 4
• Insulin drives potassium intracellularly, causing potentially fatal hypokalemia 5
• Monitor potassium closely—hypokalemia can cause respiratory paralysis, ventricular arrhythmia, and death 5
• Continue potassium supplementation until patient is stable and tolerating oral intake 3

Monitoring Without Bicarbonate

Track Resolution Using Alternative Markers

• Monitor venous pH and anion gap every 2-4 hours to assess acidosis resolution 3, 2
• Resolution criteria without bicarbonate: glucose <200 mg/dL, venous pH >7.3, and normalized anion gap 2
• If bicarbonate becomes available later, confirm it is ≥18 mEq/L for complete resolution 3, 2
• Monitor serum electrolytes, glucose, BUN, creatinine, and osmolality every 2-4 hours 3, 4

Clinical Monitoring

• Assess hemodynamic status (blood pressure improvement), fluid input/output, and mental status continuously 3, 4
• Obtain electrocardiogram to monitor for electrolyte-related cardiac effects 4

Critical Pitfalls to Avoid

Euglycemic DKA Recognition

• DKA can occur with glucose <250 mg/dL, especially with SGLT2 inhibitor use, insulin administration before arrival, or poor oral intake 2, 7
• Euglycemic DKA patients have 3-fold higher risk of hypoglycemia during treatment 7
• Don't dismiss DKA diagnosis based solely on glucose levels—rely on pH, anion gap, and ketones 2, 8

Differential Diagnosis

• Exclude other causes of high anion gap metabolic acidosis: lactic acidosis, salicylate toxicity, methanol/ethylene glycol ingestion, uremia, and alcoholic ketoacidosis 4
• Starvation ketosis typically has bicarbonate ≥18 mEq/L (when available) and glucose rarely >250 mg/dL 3
• Alcoholic ketoacidosis presents with normal to low glucose and clinical history of alcohol use 3

Electrolyte Management Errors

• Never start insulin if potassium <3.3 mEq/L—correct hypokalemia first 3, 5
• Recognize typical total body deficits: water 6-9 liters, sodium 7-10 mEq/kg, potassium 3-5 mEq/kg, chloride 5-13 mEq/kg 3, 4
• Avoid overly rapid fluid administration in pediatric patients (<20 years) due to cerebral edema risk 3

Insulin Management Errors

• Continue insulin infusion until anion gap normalizes, not just until glucose normalizes 6
• Ketogenesis reversal lags behind glucose correction 3, 6
• Add dextrose to fluids when glucose reaches 250 mg/dL to allow continued insulin administration 3, 6

Identifying Precipitating Causes

• Obtain complete blood count with differential, urinalysis, chest X-ray, and cultures as indicated 3, 4
• Common precipitants: infection (40%), new diabetes diagnosis (33%), insulin non-adherence, myocardial infarction 9, 8, 10
• Failure to identify and treat precipitating causes increases mortality and DKA recurrence risk 6, 10