What is the management of diabetic ketoacidosis (DKA)?

Management of Diabetic Ketoacidosis (DKA)

The management of diabetic ketoacidosis requires immediate intervention with intravenous fluids, insulin therapy, electrolyte replacement, and identification and treatment of the precipitating cause. 1

Diagnosis and Assessment

DKA is diagnosed based on:

• Hyperglycemia (glucose >250 mg/dL), although euglycemic DKA can occur
• Metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L)
• Presence of ketones in blood or urine 1

Severity classification:

Parameter	Mild	Moderate	Severe
Arterial pH	7.25-7.30	7.00-7.24	<7.00
Bicarbonate (mEq/L)	15-18	10-14	<10
Mental Status	Alert	Alert/drowsy	Stupor/coma

Essential laboratory tests:

• Glucose, arterial or venous blood gases (pH, bicarbonate)
• Serum electrolytes (including anion gap calculation)
• Blood or urine ketones
• Blood urea nitrogen, creatinine
• Complete blood count
• Electrocardiogram 1

Treatment Protocol

1. Fluid Resuscitation

• Begin with normal saline (0.9% NaCl) at 10-20 mL/kg/hour for the first hour
• Do not exceed 50 mL/kg in the first 4 hours
• Adjust fluid rate based on hemodynamic status and laboratory results
• For hyperchloremia, consider balanced crystalloids rather than 0.9% saline
• When blood glucose reaches 250-300 mg/dL, switch to 5% dextrose with 0.45% NaCl 1

2. Insulin Therapy

• Start continuous intravenous infusion of regular insulin at 0.1 units/kg/hour (5-7 units/hour for adults)
• For children: 0.1 units/kg/hour without a bolus
• Target glucose reduction: 50-75 mg/dL per hour
• Continue insulin until resolution of DKA (glucose <200 mg/dL, bicarbonate ≥18 mEq/L, venous pH >7.3) 1

3. Electrolyte Replacement

• Potassium: Replace based on serum levels
  • If K+ <3.3 mEq/L: Hold insulin and give 40 mEq/hr until >3.3 mEq/L
  • If K+ 3.3-5.2 mEq/L: Give 20-30 mEq in each liter of IV fluid
  • If K+ >5.2 mEq/L: Hold replacement, check levels frequently
• Calculate corrected sodium: For each 100 mg/dL glucose >100 mg/dL, add 1.6 mEq to sodium value 1

4. Bicarbonate Therapy

• Not recommended for routine use in DKA management
• May be considered only in severe acidosis (pH <6.9) or in cases with hemodynamic instability 1

Monitoring

• Vital signs: Every hour (heart rate, blood pressure, respiratory rate, mental status)
• Laboratory tests: Every 2-4 hours initially (electrolytes, BUN, creatinine, venous pH)
• Watch for signs of cerebral edema: headache, decreased mental status, irritability, abnormal pupillary responses, increased blood pressure with decreased heart rate
• Target decrease in serum osmolality should not exceed 3 mOsm/kg/hour 1

Indications for ICU Admission

Admit to ICU if:

• pH <7.00
• Altered mental status
• Hemodynamic instability
• Severe complications
• Severe hyperosmolarity (>320 mOsm/kg) 1

Transition from IV to Subcutaneous Insulin

• Administer basal insulin 2-4 hours before stopping intravenous insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia
• Successful transition requires overlap between IV and subcutaneous insulin 2

Resolution Criteria

DKA is considered resolved when:

• Glucose <200 mg/dL
• Bicarbonate ≥18 mEq/L
• Venous pH >7.3 1

Discharge Planning

Before discharge:

• Educate patients on diabetes self-management, glucose monitoring, and when to seek medical attention
• Review medication regimen, especially insulin administration
• Identify healthcare provider for follow-up diabetes care
• Schedule follow-up appointment to prevent recurrence 1

Special Considerations

• Euglycemic DKA: Can occur with SGLT2 inhibitor use; requires recognition and appropriate management
• Pregnancy: Requires tailored management strategies
• Chronic kidney disease: May need adjusted fluid and electrolyte management
• Heart failure: Careful fluid administration to avoid volume overload 3, 4

Common Pitfalls to Avoid

• Failing to recognize euglycemic DKA (normal glucose levels with ketoacidosis)
• Inadequate fluid resuscitation
• Premature discontinuation of insulin therapy before resolution of ketosis
• Inadequate potassium replacement despite normal initial levels
• Missing underlying precipitating factors (infection, myocardial infarction)
• Too rapid correction of serum osmolality, increasing risk of cerebral edema 1, 5, 6