What are the diagnostic criteria and treatment for Hyperosmolar Non-Ketotic State (HONK)

Diagnosis and Management of Hyperosmolar Non-Ketotic State (HONK)

Hyperosmolar Non-Ketotic State (HONK) is diagnosed by blood glucose ≥600 mg/dL, arterial pH >7.3, bicarbonate >15 mEq/L, effective serum osmolality ≥320 mOsm/kg H₂O, and mild ketonuria or ketonemia, typically presenting with altered mental status or severe dehydration. 1

Diagnostic Criteria

The definitive diagnostic criteria for HONK (also called Hyperglycemic Hyperosmolar State or HHS) include:

• Blood glucose ≥600 mg/dL
• Arterial pH >7.3
• Serum bicarbonate >15 mEq/L
• Effective serum osmolality ≥320 mOsm/kg H₂O
  • Calculation: 2[measured Na⁺ (mEq/L)] + glucose (mg/dL)/18
• Minimal ketonuria or ketonemia
• Altered mental status (stupor/coma) 1

Key laboratory tests to obtain immediately:

• Arterial blood gases
• Complete blood count with differential
• Urinalysis
• Plasma glucose
• Blood urea nitrogen
• Electrolytes
• Chemistry profile
• Creatinine levels
• Electrocardiogram
• Chest X-ray and cultures as needed 1

Treatment Protocol

1. Fluid Therapy (highest priority)

Adult patients:

• Initial fluid therapy: 0.9% NaCl at 15-20 mL/kg/h (1-1.5 L in average adult) during first hour
• After hemodynamic stabilization, adjust fluid choice based on:
  • Corrected serum sodium (for each 100 mg/dL glucose >100 mg/dL, add 1.6 mEq to sodium value)
  • Hydration status
  • Renal function
• Fluid replacement should correct estimated deficits within 24 hours
• Critical safety parameter: Change in serum osmolality should not exceed 3 mOsm/kg/h 1

Pediatric patients (<20 years):

• Initial fluid: 0.9% NaCl at 10-20 mL/kg/h
• Initial reexpansion should not exceed 50 mL/kg over first 4 hours
• Continue fluid therapy to replace deficit evenly over 48 hours
• Once stabilized: 0.45-0.9% NaCl at 1.5 times maintenance requirements 1

2. Insulin Therapy

• Verify potassium >3.3 mEq/L before starting insulin
• Adult dosing: IV bolus of regular insulin at 0.15 units/kg body weight, followed by continuous infusion at 0.1 unit/kg/h (5-7 units/h)
• If plasma glucose doesn't fall by 50 mg/dL in first hour, double insulin infusion rate hourly until steady glucose decline of 50-75 mg/h is achieved
• When glucose reaches 300 mg/dL:
  • Decrease insulin to 0.05-0.1 unit/kg/h (3-6 units/h)
  • Add 5-10% dextrose to IV fluids 1
• Continue insulin until mental status improves and hyperosmolarity resolves

3. Potassium Replacement

• Once renal function is confirmed and serum potassium is known:
• Include 20-30 mEq/L potassium in IV fluids (2/3 KCl and 1/3 KPO₄)
• Monitor serum potassium every 2-4 hours initially 1

4. Monitoring During Treatment

• Check blood glucose hourly until stable
• Monitor electrolytes, BUN, creatinine, osmolality every 2-4 hours
• Assess neurological status frequently
• Calculate corrected sodium regularly
• Monitor fluid input/output 1

Common Pitfalls and Complications

1. Cerebral edema: Avoid rapid changes in serum osmolality (>3 mOsm/kg/h) which can lead to cerebral edema, especially in pediatric patients

2. Fluid overload: Particularly dangerous in patients with cardiac or renal compromise; requires careful monitoring of cardiac, renal, and mental status

3. Hypokalemia: Can develop rapidly during insulin therapy; requires aggressive monitoring and replacement

4. Hypoglycemia: Can occur with excessive insulin administration; switch to dextrose-containing fluids when glucose approaches 300 mg/dL

5. Failure to identify precipitating causes: Common precipitants include infection, cerebrovascular accident, myocardial infarction, pancreatitis, medications (corticosteroids, thiazides, sympathomimetics), or medication non-adherence 1, 2

Transition to Subcutaneous Insulin

Once HONK resolves (glucose <300 mg/dL, mental status improved, osmolality normalized):

• Continue IV insulin for 1-2 hours after starting subcutaneous insulin
• Many patients with HONK may not require long-term insulin therapy and can be managed with diet or oral agents after recovery 2

HONK carries significant mortality risk, with mortality rates higher than those of diabetic ketoacidosis. Prompt recognition and aggressive management following the above protocol are essential to improve outcomes.