Endocrine Emergencies

Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) represent two life-threatening complications of uncontrolled diabetes. DKA primarily occurs in patients with type 1 diabetes due to an absolute insulin deficiency. It typically presents with hyperglycemia, ketosis, high anion gap metabolic acidosis, and dehydration, though it can occur with near-normal blood glucose. Hallmark clinical signs of DKA include rapid, deep Kussmaul respirations, a fruity or acetone breath odor, nausea, vomiting, and abdominal pain. In contrast, HHS occurs primarily in patients with type 2 diabetes who retain enough endogenous insulin to suppress lipolysis and ketogenesis. As a result, HHS is characterized by severe hyperglycemia, profound serum hyperosmolality, and severe dehydration without significant ketoacidosis. Because of this extreme serum hyperosmolality, neurological deficits, such as altered mental status, lethargy, seizures, or coma, are far more prominent in HHS than in DKA.

Initial fluid resuscitation for both DKA and HHS uses an isotonic crystalloid, such as 0.9% sodium chloride or a balanced crystalloid, to restore intravascular volume. Continuous intravenous regular insulin is commonly used for both conditions, although selected patients with mild or moderate DKA can receive subcutaneous rapid-acting insulin. Before initiating intravenous insulin, the nurse must check the serum potassium level. Under current consensus guidance, insulin must be delayed if serum potassium is below 3.5 mEq/L while potassium is actively replaced. Insulin promotes the intracellular shift of potassium, which causes serum potassium levels to decline during therapy. To prevent dangerous hypokalemia, potassium is generally added to intravenous fluids once serum potassium falls below approximately 5.0 mEq/L, provided renal function and urine output are adequate; potassium replacement should not wait until levels drop below normal.

As glucose levels normalize, management shifts to prevent sudden osmotic shifts. Under current consensus guidance, add dextrose to intravenous fluids when glucose falls below approximately 250 mg/dL in DKA or HHS, while adjusting treatment to the patient's glucose and osmolality trends. This critical addition allows intravenous insulin to continue while avoiding hypoglycemia and an overly rapid fall in plasma osmolality. A rapid reduction of serum glucose and plasma osmolality increases the risk of cerebral edema, especially in pediatric and adolescent patients. Sodium bicarbonate is not routinely recommended in DKA but may be considered for severe acidemia, generally when blood pH is below 7.0. Successful DKA resolution is assessed by the clearance of ketones and correction of acidosis, not by glucose reduction alone; while anion gap closure can be supportive, it is not the sole criterion for resolution.