The most appropriate management for this patient's hypoglycemia is to decrease insulin glargine and insulin aspart. The glucose toxicity present at the time of diabetic ketoacidosis has diminished with an intensive insulin regimen. Her remaining functional pancreatic beta cells have regained the ability to produce some insulin in the “honeymoon” phase, which explains the hypoglycemia on previously well-tolerated doses of insulin. The decreased need for insulin will not be long term as pancreatic beta cells continue to be destroyed over the course of type 1 diabetes. Continuing insulin, even at low doses, is recommended during the “honeymoon” phase in order to preserve beta cell function as long as possible by reducing the metabolic stress on these cells. The low-dose insulin regimen can consist of a basal and prandial insulin combination or a basal insulin regimen. She is experiencing symptomatic postprandial and fasting hypoglycemia. Decreasing the insulin aspart and insulin glargine doses would address the prandial and fasting hypoglycemia, while also still providing low-dose insulin to protect the functioning beta cells. She will require close monitoring of her blood glucose levels to determine when insulin doses should be increased as she nears the end of the “honeymoon” phase. The “honeymoon” period may persist for several weeks to months.
Meal-time insulin doses are generally reduced by 50% when pramlintide is initiated due to the risk of hypoglycemia. The addition of pramlintide would likely exacerbate the current issue of hypoglycemia even with reduction of meal-time insulin.
The use of sliding-scale insulin without basal insulin is discouraged. When sliding-scale insulin is used without basal insulin, the likelihood of wide swings from hyperglycemia to hypoglycemia increases. Without a basal insulin regimen, she may not consistently receive daily insulin to decrease the metabolic stress on her functioning pancreatic beta cells.
Discontinuation of both insulin glargine and insulin aspart increases metabolic stress on the pancreatic beta cells and accelerates the loss of functional cells producing insulin. As pancreatic beta cell function declines toward the end of the “honeymoon” phase, the risk of diabetic ketoacidosis increases without any exogenous insulin.