This study confirmed the well known, highly correlated relationship between POC blood glucose and HbA1c. Rohlfing et al [17] previously documented a strong relationship (R = 0.82) between blood glucose and HbA1c in patients enrolled in the Diabetes Control and Complications Trial. Nathan et al [18]also documented a strong relationship (R= 0.84) between HbA1c and average blood glucose that was consistent across diverse populations. This study’s findings show odds for SGC based on admission blood glucose followed a very similar trend as HbA1c, and both factors showed much greater odds for SGC than steroid use, independent of other factors.
Admission blood glucose was the second best predictor of SBC using regression modeling (Table 2) and the strongest predictor using classification tree analysis. Odds for SGC were both very high and remarkably similar for a concomitant range of admission blood glucose and HbA1c values (Figure). The overlapping admission blood glucose range was 165 to 240 mg/dL, which corresponded to HbA1c values between 6.65 and 8.5 (49 mmol/mol–69 mmol/mol). The odds for SGC increased from a 6.5-fold increase in odds at 165 mg/dL to 22-fold increased odds at 240 mg/dL. This corresponded to a 5.5-fold increase in odds with HbA1c of 6.65 (49 mmol/mol) to a 19-fold increase in odds with HbA1c of 8.5 (69 mmol/mol).
Notably, an admission blood glucose as low as 164 mg/dL significantly increased the odds of SGC. This relatively mild hyperglycemia is not typically considered a signifier for difficult inpatient glycemic management. Furthermore, the odds of SGC continue to increase until admission blood glucose reached approximately 240 mg/dL, at which point the odds start declining (Figure). This suggests that only exceptionally elevated admission blood glucoses triggered prompt insulin treatment on admission. The data from this study suggests targeted action for an admission blood glucose as low as 164 mg/dL is just as necessary as for those admitted with a much higher blood glucose to ensure optimal glycemic control throughout hospitalization. Implications are that admission blood glucose may be an inexpensive, straightforward, and readily available predictor of SGC and marker for targeted clinical action, especially for hospitals that do not routinely order HbA1c labs during hospitalization.
Steroid treatment was the third strongest predictor of SGC. Additional analysis showed that any proportion of hospital stay with steroid administration resulted in a stable threefold increased odds for SGC, adjusting for other predictive factors (Figure). Developing insulin treatment therapies that are tailored to patients that will be administered steroids at any point during their hospitalization may be a reasonable strategy to reduce SGC in this population. Based on the results of this study and other Sharp data, Sharp is currently piloting a steroid insulin order set that is available in the electronic health record to hospital physicians for use with any patient that is administered steroids. The order set includes eating and non-eating standards, intensified meal dose coverage, a lower blood glucose threshold for starting correction dosing, and a diabetic nurse educator consult. Evaluation will include appropriate order set usage, rate of glycemic control and extreme blood glucose values.