Pathophysiology
DKA: severe insulin deficiency. Hyperglycemia (250-600), ketosis, metabolic acidosis (pH <7.30, HCO3 <18). Mainly T1DM. Triggers: infection, missed insulin, new-onset, MI. HHS: hyperglycemia >600 without ketosis, hyperosmolality >320. Mainly T2DM.
Management
Fluids first: 0.9% NaCl 15-20 mL/kg/hr. Insulin: regular drip 0.1 units/kg/hr, titrate to glucose drop 50-75 mg/dL/hr. Add dextrose when glucose 200 (DKA) or 300 (HHS). Potassium: check before insulin. If 3.3-5.2, add 20-30 mEq KCl. If <3.3, hold insulin until corrected.
Complications
Cerebral edema (children, rapid correction). Hypokalemia (insulin shifts K intracellularly). Hypoglycemia. ARDS. Thromboembolism. Transition to SC insulin when anion gap closes, glucose <200, patient eating.
Important Notes
- Check potassium BEFORE starting insulin — insulin drives K intracellularly, causing life-threatening hypokalemia.
- Glucose should not drop >50-75 mg/dL per hour — rapid correction risks cerebral edema.
Clinical Tips
- Anion gap = Na - (Cl + HCO3) — normal 8-12. Closing gap means DKA resolving.
- Transition IV to SC: overlap 1-2h (give SC insulin, turn off drip after meal).
Summary
DKA/HHS management requires IV fluids first, then insulin infusion, aggressive potassium monitoring, and gradual glucose correction.
