Treatment of Hyperglycemic Encephalopathy
The cornerstone of treating hyperglycemic encephalopathy (hyperglycemic hyperosmolar state/HHS) is aggressive fluid resuscitation followed by insulin therapy, with careful monitoring to prevent cerebral edema from overly rapid correction of osmolality.
Initial Fluid Resuscitation
Fluid replacement is the primary initial intervention and takes precedence over insulin therapy. 1
- Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/h during the first hour to restore circulatory volume and tissue perfusion 1
- Total body water deficit in HHS typically reaches 9 liters (approximately 100-200 mL/kg) 1
- Correct estimated fluid deficits within 24 hours, ensuring serum osmolality does not decrease faster than 3 mOsm/kg/h to prevent cerebral edema 1
- After initial volume restoration and hemodynamic stabilization, transition to 0.45% NaCl (hypotonic saline) for ongoing rehydration 2
Insulin Therapy
Delay insulin administration until after initial fluid resuscitation has begun and hypokalemia is excluded. 1, 3
- Administer intravenous bolus of regular insulin at 0.15 U/kg body weight, followed by continuous infusion at 0.1 U/kg/h 1
- If plasma glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion rate hourly until achieving a steady decline of 50-75 mg/dL per hour 1
- When blood glucose reaches 250-300 mg/dL, add 5% dextrose to IV fluids while continuing insulin infusion at a reduced rate 1
- Continue insulin infusion until mental status improves and hyperosmolarity resolves 1
Electrolyte Management
Potassium replacement is critical and should begin once renal function is confirmed and serum potassium is known. 1
- Add 20-40 mEq/L potassium to the infusion once adequate urine output is established 1
- Total body deficits typically include: sodium 5-15 mEq/kg, potassium 4-6 mEq/kg, chloride 5-13 mEq/kg, and phosphate 3-7 mmol/kg 1
- Consider phosphate replacement (20-30 mEq/L potassium phosphate) in patients with cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL 1
- Correct serum sodium for hyperglycemia by adding 1.6 mEq to the measured sodium value for each 100 mg/dL glucose above 100 mg/dL 1
Monitoring Requirements
Frequent laboratory monitoring is essential to guide therapy and detect complications early. 4, 1
- Draw blood every 2-4 hours for serum electrolytes, glucose, blood urea nitrogen, creatinine, and osmolality 4, 1
- Monitor fluid input/output, vital signs, and hemodynamic parameters continuously 1
- Watch for signs of cerebral edema: lethargy, behavioral changes, seizures, incontinence, pupillary changes, bradycardia, or respiratory arrest 1
- Venous pH monitoring is adequate; repeat arterial blood gases are generally unnecessary 4
Transition to Subcutaneous Insulin
Proper timing of the transition from IV to subcutaneous insulin prevents rebound hyperglycemia. 4, 1
- Administer basal subcutaneous insulin 2-4 hours before discontinuing IV insulin infusion 4, 1
- This overlap prevents recurrence of hyperglycemia and metabolic decompensation 4
Critical Pitfalls to Avoid
- Do not administer bicarbonate - it does not improve outcomes in HHS and is not indicated 1
- Avoid overly rapid correction of hyperglycemia and osmolality - this increases risk of cerebral edema, particularly in pediatric patients 1, 5
- Do not use sliding scale insulin alone - continuous IV insulin infusion is the standard of care for critically ill patients 4
- Never start insulin before excluding hypokalemia - insulin drives potassium intracellularly and can precipitate life-threatening hypokalemia 4, 1
Identification of Precipitating Causes
Simultaneously investigate and treat underlying triggers while managing the metabolic crisis. 1