Initial Laboratory Evaluation and Management for Diabetic Ketoacidosis
Immediately obtain arterial blood gases, complete blood count with differential, comprehensive metabolic panel (electrolytes, BUN, creatinine, glucose), serum or urine ketones (preferably β-hydroxybutyrate), urinalysis, and electrocardiogram upon presentation. 1, 2
Essential Initial Laboratory Tests
Core Diagnostic Labs
- Arterial blood gases: Document metabolic acidosis with pH <7.3 1, 2
- Serum glucose: Typically >250 mg/dL in classic DKA, though euglycemic variants exist with glucose <250 mg/dL 2, 3
- Serum bicarbonate: Confirm levels <15-18 mEq/L 1, 2, 4
- Serum ketones: Measure β-hydroxybutyrate specifically (the predominant ketone in DKA), as nitroprusside-based tests do not measure this and should not be used for monitoring 2
- Electrolytes with calculated anion gap: Document high anion gap metabolic acidosis (>10 mEq/L in mild DKA, >12 mEq/L in moderate-severe) 2, 4
- BUN/creatinine: Assess renal function and hydration status 2
Supporting Laboratory Tests
- Complete blood count with differential: Evaluate for underlying infection as a precipitating factor 1, 2
- Urinalysis with urine ketones by dipstick: Provides supporting evidence but should not be used alone for diagnosis 2
- Serum osmolality: Calculate to help differentiate from other causes of acidosis 2
- Hemoglobin A1C: Assess chronic glycemic control 3
- Electrocardiogram: Identify cardiac complications and monitor for electrolyte abnormalities 3
Additional Tests Based on Clinical Presentation
- Blood and urine cultures: If infection is suspected as precipitating cause 1
- Chest radiography: When pneumonia or other pulmonary pathology is suspected 1, 3
- Amylase, lipase, hepatic transaminases: Consider if abdominal pain is prominent 3
- Troponin, creatine kinase: If cardiac ischemia is suspected 3
- Serum lactate, salicylate, methanol levels: When other causes of high anion gap acidosis are suspected 1, 2
Critical Diagnostic Pitfalls to Avoid
- Do not rely on urine ketone testing alone: It is insufficient for diagnosis and may be misleading 2
- Do not use nitroprusside-based blood ketone tests for monitoring treatment: They do not measure β-hydroxybutyrate, the predominant ketone 2
- Do not dismiss DKA based on glucose <250 mg/dL: Euglycemic DKA is increasingly common, especially with SGLT-2 inhibitor use 2, 3, 5
- Correct serum sodium for hyperglycemia: Add 1.6 mEq/L to the measured sodium value for each 100 mg/dL glucose above 100 mg/dL 1
Typical Electrolyte and Fluid Deficits
The average adult with DKA presents with total body deficits of 1:
- Water: 6-9 liters (100 ml/kg)
- Sodium: 7-10 mEq/kg
- Potassium: 3-5 mEq/kg
- Chloride: 5-13 mEq/kg
- Phosphate: 3-5 mmol/kg
- Magnesium: 4-6 mEq/kg
- Calcium: 1-2 mEq/kg
Initial Management Protocol
Fluid Resuscitation (First Hour)
Administer isotonic saline (0.9% NaCl) at 15-20 ml/kg/hour during the first hour (1-1.5 liters in the average adult) in the absence of cardiac compromise. 1, 6
Subsequent Fluid Management
- If corrected serum sodium is normal or elevated: Use 0.45% NaCl at 4-14 ml/kg/hour 1
- If corrected serum sodium is low: Continue 0.9% NaCl at 4-14 ml/kg/hour 1
- Target: Correct estimated deficits within 24 hours, with serum osmolality change not exceeding 3 mOsm/kg H₂O per hour 1
Potassium Replacement
Once renal function is assured, add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO₄) until the patient is stable and can tolerate oral supplementation. 1, 6
Monitoring Requirements
- Vital signs, fluid input/output, and mental status: Continuous assessment 6
- Electrolytes, glucose, and acid-base status: Serial measurements every 2-4 hours 4
- Hemodynamic monitoring: Track improvement in blood pressure 1
- In patients with renal or cardiac compromise: Frequent assessment of serum osmolality and cardiac, renal, and mental status to avoid iatrogenic fluid overload 1
Pediatric Considerations (<20 Years)
Initial fluid therapy in children should be isotonic saline (0.9% NaCl) at 10-20 ml/kg/hour during the first hour, with careful attention to the risk of cerebral edema associated with rapid fluid administration. 1
Differential Diagnosis Considerations
Exclude other causes of high anion gap metabolic acidosis 1, 2, 4:
- Lactic acidosis
- Salicylate toxicity
- Methanol or ethylene glycol ingestion (look for calcium oxalate and hippurate crystals in urine)
- Uremia
- Alcoholic ketoacidosis (distinguished by recent alcohol cessation, glucose rarely >250 mg/dL, and β-hydroxybutyrate elevation)