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DKA Management - Harrison's Principles of Internal Medicine, 22nd Edition (2025)

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Classification of DKA Severity

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Laboratory Values at Presentation (Table 416-7)

Euglycemic DKA (seen with SGLT2 inhibitor use): glucose 100-250 mg/dL, pH <7.3, ketones ++.

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Management Protocol (Table 416-9)

1. Confirm Diagnosis

• Elevated serum glucose
• Elevated serum beta-hydroxybutyrate
• Metabolic acidosis

2. Admission

• ICU for severe DKA
• Step-down unit with close monitoring for mild-moderate DKA

3. Initial Assessment

• Serum electrolytes: K+, Na+, Mg2+, Cl-, HCO3-, phosphate
• Acid-base status: pH, HCO3-, PCO2, beta-hydroxybutyrate
• Renal function: creatinine, urine output

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4. Fluid Replacement

• 0.9% saline or Lactated Ringer's 2-3 L at 10-20 mL/kg/hour
• Ringer's lactate is associated with more rapid DKA resolution and reduced risk of hyperchloremia compared to normal saline

• Switch to 0.45% saline at 250-500 mL/hour

• Change to 5-10% glucose + 0.45% saline or Ringer's lactate at 150-250 mL/hour
• Total fluid deficit is typically 3-5 L, replaced over 24 hours

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5. Insulin

• Bolus: 0.1 units/kg IV of short-acting regular insulin
• Then 0.1 units/kg/hour continuous IV infusion
• If no response in 2-4 hours, increase 2 to 3-fold

• 0.1 unit/kg rapid-acting insulin analogue SC, then 0.1 unit/kg every 1 hour
• OR 0.2 unit/kg every 2 hours

• Do NOT discontinue IV insulin until 1-2 hours after the first SC insulin dose is given (to avoid rebound ketosis)
• Continue IV insulin until glucose is <200 mg/dL AND the patient can eat

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6. Potassium

• Initial K+ is often normal or elevated (due to acidosis shifting K+ extracellularly), but total body potassium is depleted
• If K+ <3.5 meq/L: Hold insulin; replace KCl at 40 meq/hour until K+ ≥3.5
• If K+ 3.5-5.0 meq/L: Add 20-30 meq K+ per liter of IV fluid
• If K+ >5.0 meq/L: Do not add potassium; monitor every 2 hours

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7. Bicarbonate

• Generally not recommended for most DKA patients
• Consider if pH <7.0: 100 mmol NaHCO3 in 400 mL sterile water + 20 meq KCl over 2 hours
• Risks: paradoxical CNS acidosis, worsening hypokalemia, delayed ketone clearance

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8. Phosphate

• Routine phosphate replacement is not recommended
• Consider supplementation if serum phosphate <1.0 mg/dL, cardiac dysfunction, or respiratory depression

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9. Monitoring

• A comprehensive flow sheet is essential: vital signs, fluid intake/output, insulin administered, and lab values on a chronologic basis
• Glucose should be checked every 1-2 hours
• Electrolytes every 2-4 hours
• Watch for signs of cerebral edema - most common in children, extremely serious

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10. Identifying and Treating the Precipitant

• Infection (most common) - look for signs even without fever
• Missed/insufficient insulin doses
• Physiologic stress (surgery, trauma, MI)
• SGLT2 inhibitor use (euglycemic DKA)

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11. Transition and Follow-up

• After resolution, resume long-acting (basal) insulin before stopping IV insulin
• Review the sequence of events that led to DKA - patient education is key
• DKA can be recurrent, sometimes indicating underlying mental health issues, insulin cost barriers, or social determinants of health
• Even a single episode of DKA is associated with greatly increased 1-year mortality

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Clinical Pearls from Harrison's

• Nausea/vomiting in a diabetic patient always warrants DKA workup
• Abdominal pain can mimic acute pancreatitis or ruptured viscus
• Kussmaul respirations + fruity breath = classic signs
• Apparent normokalemia or hyperkalemia at presentation masks severe total body K+ depletion - K+ will fall rapidly with insulin
• If the patient is vomiting or has altered mental status, insert a nasogastric tube to prevent aspiration
• Failure to augment insulin during physiologic stress often precipitates DKA in established diabetics
• Harrison's Principles of Internal Medicine, 22E (2025), Chapter 416, pp. 3260-3261