Fluid replacement is of paramount importance in treating nonketotic hyperglycemic coma. The onset of hyperosmolarity is more insidious in elderly people without ketosis than in younger individuals with high serum ketone levels, which provide earlier indicators of severe illness (vomiting, rapid deep breathing, acetone odor, etc). Consequently, diagnosis and treatment are often delayed until fluid deficit has reached levels of 6–10 L.
If hypovolemia is present as evidenced by hypotension and oliguria, fluid therapy should be initiated with 0.9% saline. In all other cases, 0.45% saline appears to be preferable as the initial replacement solution because the body fluids of these patients are markedly hyperosmolar. As much as 4–6 L of fluid may be required in the first 8–10 hours. Careful monitoring of the patient is required for proper sodium and water replacement. An important end point of fluid therapy is to restore urinary output to 50 mL/h or more. Once blood glucose reaches 250 mg/dL (13.9 mmol/L), fluid replacement should include 5% dextrose in either water, 0.45% saline solution, or 0.9% saline solution. The rate of dextrose infusion should be adjusted to maintain glycemic levels of 250–300 mg/dL (13.9–16.7 mmol/L) in order to reduce the risk of cerebral edema.
Less insulin may be required to reduce the hyperglycemia in nonketotic patients as compared to those with diabetic ketoacidotic coma. In fact, fluid replacement alone can reduce hyperglycemia considerably by correcting the hypovolemia, which then increases both glomerular filtration and renal excretion of glucose. Insulin treatment should therefore be delayed unless the patient has significant ketonemia (beta-hydroxybutyrate more than 1 mmol/L). Start the insulin infusion rate at 0.05 unit/kg/h (bolus is not needed) and titrate to lower blood glucose levels by 50–70 mg/dL per hour (2.8–3.9 mmol/L/h). Once the patient has stabilized and the blood glucose falls to around 250 mg/dL (13.9 mmol/L), insulin can be given subcutaneously.
With the absence of acidosis, there may be no initial hyperkalemia unless associated end-stage chronic kidney disease is present. This results in less severe total potassium depletion than in DKA, and less potassium replacement is therefore needed. However, because initial serum potassium is usually not elevated and because it declines rapidly as a result of insulin’s effect on driving potassium intracellularly, it is recommended that potassium replacement be initiated earlier than in ketotic patients, assuming that no chronic kidney disease or oliguria is present. Potassium chloride (10 mEq/L) can be added to the initial bottle of fluids administered if the patient’s serum potassium is not elevated.
If severe hypophosphatemia (serum phosphate less than 1 mg/dL [0.32 mmol/L]) develops during insulin therapy, phosphate replacement can be given as described for ketoacidotic patients (at 3 mmol/h).