Sliding Scale Insulin—Time to Stop Sliding

Abstract

IN MOST TEACHING HOSPITALS IN THE UNITED STATES, PRImary care first-year residents and medical students learn about sliding scale insulin (SSI), usually from a senior resident. The more experienced resident explains how to prescribe regular insulin every 4 to 6 hours without any scheduled basal or mealtime (prandial) insulin. For the typical patient who is too sick to eat, this results in a roller coaster effect on blood glucose variability due to poor matching of insulin with individual blood glucose patterns. Unfortunately, for the patient who is able to eat, insulin scheduled to be administered based on a bedside capillary glucose measurement is actually administered long after the meal is consumed. Although there are often challenges with hospital logistics in terms of timing of insulin administration in relation to actual food intake, the SSI orders typically do not mention the relationship of the insulin injection as it pertains to a meal, even though at one time, the resident was taught that regular insulin is mealtime insulin. Even worse, SSI, as used here, does not account for the basic principles of insulin therapy. Certainly, SSI has evolved considerably since first described by Joslin more than 70 years ago. For decades, insulin doses were based on the amount of glycosuria (fractional urine glucose testing) for both inpatient and outpatient settings. Although glycosuria is no longer used for this indication, there is still the fundamental problem of clinicians and even health care systems having nonstandardized definitions of SSI. Usually, SSI involves use of regular insulin or a rapid-acting insulin analogue provided without any other scheduled short-acting or long-acting insulin, but there are variations. For example, in one recent study, SSI was defined as regular insulin provided prior to meals and at bedtime based on bedside blood glucose testing or every 6 hours for the patient who is not eating. Both clinicians and patients often refer to the use of SSI as the addition of insulin to previously scheduled prandial insulin. So how can the merits or inadequacies of SSI be discussed when they cannot even be defined? Strategies that do not mimic normal insulin secretion (nonphysiologic regimens such as basal insulin at bedtime only) can also result in different patient outcomes based on the type of diabetes. With the more common type 2 diabetes mellitus manifested by insulin resistance and relative insulin deficiency, long periods of insulin deficiency or even insulin stacking (when insulin doses are injected at times too close together, resulting in an overlap of action of the insulin) will usually not result in any metabolic crisis. However, in patients with type 1 diabetes mellitus, who generally are not resistant to insulin and have complete insulin deficiency, SSI is more apt to result in clinically significant hyperglycemia, ketosis, ketoacidosis, or hypoglycemia. No data are available for how often this happens but experienced clinicians have observed this repeatedly over the years. Perhaps the lack of major clinical crises when SSI is used in type 2 diabetes mellitus helps to fuel its acceptance in our medical culture. Surprisingly, there are not more clinical trials assessing the efficacy and safety of SSI. One randomized controlled trial reported superior glycemic control of a more physiologic basal-bolus (replacing both background and mealtime) insulin therapy compared with SSI, but the SSI group received a much lower dose of daily insulin (12.5 U/d vs 42 U/d for basal-bolus), potentially biasing the results. Nevertheless, inpatient diabetes therapy has gained interest this decade due to both interventional and observational studies, suggesting that hyperglycemia in hospitalized patients can result in deleterious outcomes. There is also increasing literature to support that hypoglycemia in the inpatient setting, especially for critically ill patients, is more dangerous than originally appreciated. Appropriate insulin nomenclature includes 3 components: basal insulin (inhibits hepatic glucose production overnight and between meals), prandial (also called bolus or mealtime) insulin (promotes glucose disposal into muscles from food consumption), and correction-dose insulin. This latter component is often confused with SSI, yet it is quite different. Correction-dose insulin is usually administered as an addition (or supplement) to the usual dose of mealtime insulin as a specific algorithm based on total daily dose of insulin or patient weight. SSI is defined (for the purpose of this Commentary) as it is used in the traditional sense: an