Effect of intravenous glucocorticoids on the efficiency of tight glycaemic control
- 617 Downloads
KeywordsBlood Glucose Level Intensive Insulin Therapy Blood Glucose Measurement Patient Data Management System Tight Glycaemic Control
Intravenous glucocorticoids (GC) are often administered during critical illness in the context of post-transplant immunosuppression, ARDS, septic shock or severe inflammatory vasoplegia. As a counter-regulatory hormone of insulin, GC may interfere substantially with tight glycaemic control to normal for age blood glucose levels by intensive insulin therapy. Therefore we hypothesized that the first administration of an intravenous GC gives rise to significant hyperglycaemia and that the effect is more pronounced for the synthetic GC.
All patients admitted to the surgical and paediatric ICU between 1 July 2008 and 1 July 2009 were screened for intravenous glucocorticoid use in our patient data management system. In those patients, arterial blood glucose levels, all measured by blood gas analyzer, within the time frame of 48 hours surrounding the GC administration were retrieved. Up to two baseline blood glucose levels (before GC administration) and up to six blood glucose levels post administration were analysed by repeated-measures ANOVA. Data are expressed as mean ± SD or as median (IQR).
A total of 452 patients - n = 26 (<1 year), n = 76 (1 to 17 years), n = 350 (>17 years) - received intravenous GC: hydrocortisone 32%, bolus methylprednisolone 52%, drip methylprednisolone 4% and dexamethasone 12%. Baseline blood glucose levels were 97 ± 34 mg/dl (<1 year), 104 (89 to 132) mg/dl (1 to 17 years), 136 (106 to 174) mg/dl (>17 years). In the adult patients the first blood glucose measurement was 1.0 (0.4 to 2.0) hours after GC administration. Blood glucose levels decreased over time from baseline after GC administration (P < 0.0001). The sixth glycaemia was 110 (91 to 139) mg/dl taken 12.4 (9.6 to 16.5) hours after GC administration. This decrease of glycaemia was only present in patients who received 92 ± 35 mg hydrocortisone (P = 0.004) or 40 (20 to 125) mg bolus methylprednisolone (P < 0.0001). In patients who received 113 (71 to 160) mg drip methylprednisolone (P = 0.14) or 10 (5 to 12.5) mg dexamethasone (P = 0.44), blood glucose levels did not change over time.
We showed that, when a tight blood glucose protocol is implemented, intravenous GC administration does not necessarily lead to an increase in blood glucose level. The blood glucose profile after methylprednisolone or dexamethasone administration did not differ from the glycaemic response after hydrocortisone administration. However, avoiding hyperglycaemic peaks after the GC administration during tight glycaemic control requires an on average 2-hourly blood glucose measurement.