A nurse is monitoring a client receiving a continuous intravenous regular insulin infusion for severe hyperglycemia and metabolic acidosis. The client's most recent blood glucose level has dropped significantly to 240 mg/dL. Which intervention should the nurse anticipate next to prevent complications?

When managing severe hyperglycemia and metabolic acidosis (such as in diabetic ketoacidosis, DKA) with a continuous intravenous regular insulin infusion, the primary goal is to resolve the ketosis and acidosis, not just to lower the blood glucose. The insulin infusion is the cornerstone of this treatment because it suppresses lipolysis and ketogenesis. A blood glucose level of 240 mg/dL indicates that the insulin is effective, but the underlying metabolic crisis is not yet resolved. If the insulin infusion is stopped or reduced prematurely, ketone production will resume, and the acidosis will worsen.

The most critical complication to prevent at this stage is hypoglycemia and the subsequent rebound ketosis that can occur if the insulin infusion is discontinued. The standard of care, as reflected in major consensus guidelines for DKA management, is to transition to a dextrose-containing fluid once the blood glucose falls to around 200–250 mg/dL. This strategy allows the insulin infusion to continue at a rate sufficient to clear ketones and correct the anion gap, while the exogenous dextrose provides a substrate to prevent the blood glucose from dropping to dangerous levels. This prevents the nurse from having to reduce the insulin rate, which would slow the resolution of the life-threatening acidosis ^[2].

Discontinuing the insulin infusion immediately (Option 1) would halt the suppression of ketogenesis, leading to a rapid recurrence of metabolic acidosis. Increasing the rate of normal saline (Option 2) addresses volume status but does not directly manage the falling glucose level or the ongoing need for insulin to correct the acidosis. Switching to subcutaneous insulin (Option 4) is an inappropriate transition at this glucose level; the patient is still acutely acidotic and requires the precise, titratable control of an intravenous infusion. Subcutaneous insulin absorption can be erratic in a volume-depleted patient, making it an unsafe choice during the acute phase of treatment ^[2].

The pathophysiology of DKA involves an absolute or relative insulin deficiency that leads to uncontrolled hepatic glucose production and ketogenesis. The treatment with intravenous insulin directly reverses this process. However, as the blood glucose normalizes faster than the ketones clear, a glucose source must be provided to sustain the necessary insulin dose. This concept is also relevant in understanding the risks of euglycemic DKA, a variant where blood glucose is not markedly elevated but a profound metabolic acidosis from ketones is present, often seen with SGLT2 inhibitor use. In those cases, a dextrose infusion is also a key intervention to allow for simultaneous insulin administration [2,3].

Therefore, the nurse should anticipate the addition of dextrose to the intravenous fluids. This allows the continuous insulin infusion to be maintained at the rate required to resolve the metabolic acidosis, while the dextrose prevents iatrogenic hypoglycemia during the ongoing treatment phase ^[2].