Initial ICU Management of DKA and HHS
Begin aggressive fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/h (1-1.5 L in the first hour) to restore intravascular volume and renal perfusion, followed by continuous IV insulin infusion at 0.1 units/kg/h after confirming potassium >3.3 mEq/L, with close monitoring of electrolytes every 2-4 hours. 1, 2
Pathophysiology
DKA Pathophysiology
- Absolute insulin deficiency leads to uncontrolled lipolysis and ketone body production (β-hydroxybutyrate, acetoacetate, acetone), causing metabolic acidosis with pH <7.3 and bicarbonate <15 mEq/L 3, 4
- Hyperglycemia (>250 mg/dL) results from decreased glucose utilization and increased hepatic gluconeogenesis 3
- Osmotic diuresis causes total body water deficit of approximately 6 liters (100 mL/kg) 3
HHS Pathophysiology
- Relative insulin deficiency with enough insulin to prevent ketosis but insufficient to prevent severe hyperglycemia (>600 mg/dL) 2, 3
- Profound dehydration with total body water deficit of 9 liters (100-200 mL/kg) due to prolonged osmotic diuresis 3
- Effective serum osmolality >320 mOsm/kg causes altered mental status and severe dehydration 2, 5
- Minimal ketosis distinguishes HHS from DKA (pH >7.3, bicarbonate >15 mEq/L) 3, 5
Initial Assessment and Diagnosis
Immediate Laboratory Workup
- Obtain arterial blood gases, complete blood count with differential, urinalysis, plasma glucose, BUN, electrolytes, chemistry profile, and creatinine immediately 1, 2
- Order electrocardiogram, chest X-ray, and cultures as clinically indicated to identify precipitating causes 1
- Calculate effective serum osmolality: 2[measured Na (mEq/L)] + glucose (mg/dL)/18 1, 2
- Correct serum sodium for hyperglycemia: add 1.6 mEq to sodium value for each 100 mg/dL glucose above 100 mg/dL 1, 2
Diagnostic Criteria
DKA: Blood glucose >250 mg/dL, arterial pH <7.3, bicarbonate <15 mEq/L, moderate ketonuria or ketonemia 1, 3
HHS: Blood glucose >600 mg/dL, arterial pH >7.3, bicarbonate >15 mEq/L, effective serum osmolality >320 mOsm/kg, altered mental status or severe dehydration 2, 3, 5
Fluid Resuscitation Protocol
First Hour
- Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/h (typically 1-1.5 L in average adult) to expand intravascular volume and restore renal perfusion 1, 2
- This aggressive initial resuscitation is critical for both conditions, though HHS requires more total fluid replacement due to greater dehydration 3
After Initial Resuscitation
- Switch to 0.45% NaCl if corrected serum sodium is normal or elevated after hemodynamic stabilization 1, 2
- Continue 0.9% NaCl if corrected serum sodium is low 1
- Target fluid replacement to correct estimated deficits within 24 hours 2, 5
Critical Safety Parameters
- Limit induced change in serum osmolality to <3 mOsm/kg/h to prevent cerebral edema 2
- Monitor fluid input/output, hemodynamic parameters, and mental status frequently during resuscitation 1, 2
- Exercise particular caution in elderly patients and those with cardiac or renal compromise 5
Glucose-Specific Fluid Adjustments
- When glucose reaches 250 mg/dL in DKA or 300 mg/dL in HHS, change to 5% dextrose with 0.45-0.75% NaCl 1, 2, 5
- Continue dextrose-containing fluids to prevent hypoglycemia while maintaining insulin therapy to resolve metabolic abnormalities 2, 5
Insulin Therapy Protocol
Pre-Insulin Requirements
- Do NOT start insulin if potassium <3.3 mEq/L - correct hypokalemia first to prevent life-threatening cardiac arrhythmias 1
- Ensure adequate fluid resuscitation has begun 6
Adult Insulin Dosing
- IV bolus: 0.15 units/kg body weight of regular insulin 1
- Continuous infusion: 0.1 units/kg/h (typically 5-7 units/h in adults) 1
- Target glucose decline of 50-75 mg/dL per hour 1
Insulin Adjustment Algorithm
- If glucose does not fall by 50 mg/dL in the first hour: verify adequate hydration, then double insulin infusion rate hourly until achieving steady glucose decline of 50-75 mg/h 1
- When glucose reaches 250 mg/dL in DKA: decrease insulin to 0.05-0.1 units/kg/h and add dextrose to IV fluids 1
- When glucose reaches 300 mg/dL in HHS: decrease insulin to 0.05-0.1 units/kg/h (3-6 units/h) 2, 5
Key Insulin Management Principles
- Continue insulin until resolution of ketoacidosis in DKA (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L), even if glucose normalizes 3
- In HHS, continue insulin until mental obtundation and hyperosmolarity resolve 2
- Ketonemia takes longer to clear than hyperglycemia - do not prematurely stop insulin based on glucose alone 1
Electrolyte Management
Potassium Replacement
- Once renal function confirmed and K+ known, add 20-40 mEq/L potassium to IV fluids 1, 2
- Use 2/3 KCl or potassium acetate and 1/3 KPO₄ 1, 2
- Target serum potassium between 4-5 mEq/L 3
- Potassium deficits are greater in HHS (5-15 mEq/kg) compared to DKA (3-5 mEq/kg) 3
Monitoring Schedule
- Check electrolytes every 2-4 hours during initial treatment 1, 2
- Monitor sodium, potassium, chloride, bicarbonate, phosphate, magnesium, glucose, BUN, creatinine, and osmolality 2, 5
- Venous pH monitoring is adequate for DKA (usually 0.03 units lower than arterial pH) - repeat arterial blood gases are generally unnecessary 1
Other Electrolytes
- Monitor and correct magnesium and phosphate abnormalities as needed 2
- Routine phosphate replacement is not recommended unless severe hypophosphatemia develops 1
Ketone Monitoring (DKA-Specific)
- β-hydroxybutyrate measurement is the preferred method for monitoring DKA resolution 1
- Avoid nitroprusside method (urine ketones) as it only measures acetoacetate and acetone, not β-hydroxybutyrate 1
- During therapy, β-hydroxybutyrate converts to acetoacetate, which may falsely suggest worsening ketosis by nitroprusside testing 1
Resolution Criteria and Transition
DKA Resolution
HHS Resolution
Transition to Subcutaneous Insulin
- Administer basal insulin 2-4 hours BEFORE stopping IV insulin to prevent rebound hyperglycemia 2, 3, 5
- This overlap period is critical - premature termination of IV insulin is a common pitfall 7
- Consider low-dose basal insulin analog given with IV insulin to prevent rebound hyperglycemia 3
Critical Complications to Monitor
Cerebral Edema
- Most common in children but can occur in adults with rapid osmolality correction 1, 2
- Prevent by limiting osmolality change to <3 mOsm/kg/h 2
- Avoid excessive fluid administration and overly rapid glucose correction 6
- Monitor mental status continuously for early detection 1, 2
Fluid Overload
- Particularly dangerous in patients with cardiac or renal compromise 1, 5
- Monitor hemodynamic parameters, lung sounds, and oxygen saturation closely 1
Hypokalemia
- Insulin therapy drives potassium intracellularly, potentially causing life-threatening hypokalemia 1
- Never start insulin if K+ <3.3 mEq/L 1
Bicarbonate Therapy
- Bicarbonate is NOT routinely recommended as it has not been shown to improve outcomes 3, 5
- Consider only if pH <6.9 or when pH <7.2 with serum bicarbonate <10 mEq/L pre/post-intubation to prevent hemodynamic collapse 6
- Bicarbonate can worsen ketosis, cause hypokalemia, and increase cerebral edema risk 6
Precipitating Factors to Address
- Identify and treat underlying causes: infection (most common), myocardial infarction, stroke, medications (diuretics, corticosteroids, beta-blockers), non-adherence to insulin 2, 5, 4
- The antibiotic choice (piperacillin-tazobactam 4.5g) mentioned in your case is appropriate for suspected infection as a precipitant 1
ICU Admission Criteria
- Cardiovascular instability 4
- Inability to protect airway 4
- Obtundation or altered mental status 4
- Acute abdominal signs suggesting gastric dilatation 4
- Need for frequent monitoring and IV insulin infusion 4
Common Pitfalls to Avoid
- Premature termination of IV insulin before complete resolution of ketoacidosis in DKA 7
- Insufficient overlap between IV and subcutaneous insulin, causing rebound hyperglycemia 7
- Starting insulin before correcting hypokalemia (K+ <3.3 mEq/L) 1
- Overly rapid correction of osmolality (>3 mOsm/kg/h), risking cerebral edema 2
- Using nitroprusside method to monitor ketone resolution in DKA 1
- Inadequate fluid resuscitation, particularly in HHS where deficits are greater 3