Management of Diabetic Ketoacidosis (DKA) in the ICU
The cornerstone of DKA management in the ICU includes aggressive fluid resuscitation, insulin therapy, electrolyte correction, and identification/treatment of underlying causes, with continuous monitoring to guide therapy adjustments. 1
Initial Assessment and Stabilization
- Perform careful clinical and laboratory assessment including plasma glucose, blood urea nitrogen, creatinine, serum ketones, electrolytes with calculated anion gap, osmolality, urinalysis, arterial blood gases, and complete blood count 1
- Identify and treat any underlying cause of DKA such as sepsis, myocardial infarction, or stroke 1
- Management goals include restoration of circulatory volume, tissue perfusion, resolution of hyperglycemia/ketoacidosis, and correction of electrolyte imbalances 1
Fluid Resuscitation
- Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour to restore circulatory volume and tissue perfusion 1
- Recent evidence suggests balanced electrolyte solutions may offer faster DKA resolution compared to normal saline 2, 3, 4
- Continue fluid replacement based on hemodynamic status, serum electrolyte levels, and urine output 1
- Monitor fluid input/output and clinical examination to assess progress with fluid replacement 1
Insulin Therapy
- In critically ill and mentally obtunded patients with DKA, continuous intravenous insulin is the standard of care 1
- For mild or moderate uncomplicated DKA, subcutaneous rapid-acting insulin analogs may be used when combined with aggressive fluid management 1
- Monitor blood glucose every 2-4 hours while the patient takes nothing by mouth and adjust insulin dosing accordingly 1
- When transitioning from intravenous to subcutaneous insulin, administer basal insulin 2-4 hours before stopping the intravenous insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia 1
- A low dose of basal insulin analog in addition to intravenous insulin infusion may prevent rebound hyperglycemia without increased risk of hypoglycemia 1
Electrolyte Management
- Monitor potassium levels closely as total body potassium deficits are common despite potentially normal or elevated initial serum levels due to acidosis 1
- Once renal function is assured and serum potassium is known, add 20-40 mEq/L potassium to the infusion when serum levels fall below 5.5 mEq/L 1
- Monitor and replace other electrolytes including phosphate, magnesium, and calcium as needed 1
- Bicarbonate administration is generally not recommended as studies have shown it makes no difference in resolution of acidosis or time to discharge 1
Monitoring for Resolution
- During therapy, blood should be drawn every 2-4 hours to determine serum electrolytes, glucose, blood urea nitrogen, creatinine, and osmolality 1
- Treatment success is indicated by resolution of acidosis (pH >7.3), serum bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L, and improvement in clinical symptoms 1
- Direct measurement of β-hydroxybutyrate in blood is preferred for monitoring DKA resolution 5
Transition from ICU and Discharge Planning
- A structured discharge plan should be tailored to the individual patient to reduce length of hospital stay and readmission rates 1
- Discharge planning should begin at admission and be updated as patient needs change 1
- Schedule follow-up appointments prior to discharge to increase the likelihood that patients will attend 1
- Review key areas of knowledge before discharge including identification of diabetes care provider, blood glucose monitoring, recognition and treatment of hyperglycemia/hypoglycemia, and medication administration 1
Common Pitfalls and Caveats
- Inadequate fluid resuscitation can delay recovery and worsen outcomes 1
- Premature discontinuation of insulin therapy before complete resolution of ketosis can lead to recurrence of DKA 1
- Failure to monitor and replace electrolytes can lead to complications, particularly cardiac arrhythmias 1
- Not identifying or treating the underlying cause of DKA can lead to treatment failure 1
- Be aware of euglycemic DKA, particularly in patients taking SGLT2 inhibitors, where ketoacidosis occurs without marked hyperglycemia 5, 6