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Communications to the Editor |

Relationship of Baseline Glucose and Mortality During Medical Critical Illness? FREE TO VIEW

Jack J. M. Ligtenberg, MD, PhD; Sofie Meijering, MD; Mathijs Vogelzang; Maarten W. N. Nijsten, MD, PhD; Iwan C. C. van der Horst, MD; Jaap E. Tulleken, MD, PhD; Jan G. Zijlstra, MD, PhD
Author and Funding Information

University Medical Center, Groningen, the Netherlands

Correspondence to: Jack J. M. Ligtenberg, MD, Intensive and Respiratory Care Unit (ICB), University Medical Center, PO Box 30.001, NL-9700 RB Groningen, the Netherlands; e-mail: j.j.m.ligtenberg@int.azg.nl



Chest. 2005;127(6):2283. doi:10.1378/chest.127.6.2283
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To the Editor:

We read with interest the study by Cely et al (September 2004)1 on the relationship of baseline glucose homeostasis to hyperglycemia in critically ill patients. The authors show that hyperglycemia generally is present in critical illness, and that patients with low “baseline” hemoglobin-A1c levels are less inclined to hyperglycemia than patients with higher hemoglobin-A1c levels. Furthermore, they mention that “patients with normal and abnormal baseline glucose control had similar survival rates.” We don’t think that this statement has statistical validity, considering the limited number of evaluated patients (75 patients; ICU mortality rate, 29%).

To determine the relation between blood glucose regulation and mortality, we conducted an analysis among all patients admitted to our medical ICU over a 2-year period. A total of 1,209 consecutive patients were included. ICU mortality was 19.4%. A total of 10,954 glucose measurements were obtained. Mortality was significantly lower in the group with a mean glucose level of 4.0 to 6.0 mmol/L vs the group with a mean glucose level of 6.0 to 10.0 mmol/L: 12% vs 17.6% (p = 0.03). Patients who died in the ICU (n = 235) also had significantly higher baseline glucose values than patients who left the ICU alive (n = 974): 9.0 ± 5.3 mmol/L vs 7.6 ± 4.3 mmol/L (mean ± SD). We also calculated mortality rate after classifying patients into groups based on average glucose levels during ICU admission. The mortality rate in the group with an average glucose level of 4.4 to 6.1 mmol/L (n = 300) was 12%, while mortality with an average glucose level of > 11.1 mmol/L (n = 96) was 37.5%. Maximal glucose values during hospital admission appeared to be lower in survivors than in nonsurvivors: 9.6 ± 5.2 mmol/L vs 11.7 ± 6.0 mmol/L, respectively).

Acute hyperglycemia is frequently found in stress situations.2Since it is so common, it could be explained as a physiologic adaptation. However, hyperglycemia is associated with complications, and there is increasing evidence that strict regulation of glycemia could have beneficial effects on morbidity and even mortality.3

Based on our own findings and those of others, we assume that hyperglycemia is correlated with mortality in critically ill patients. The next important step is to design and start up feasible glucose regulation protocols and study the effect of strict glucose control also in medical intensive care patients.

Cely, CM, Arora, P, Quartin, AA, et al (2004) Relationship of baseline glucose homeostasis to hyperglycemia during medical critical illness.Chest126,879-887. [CrossRef] [PubMed]
 
van der Horst, IC, Ligtenberg, JJ, Bilo, HJ, et al Glucose-insulin-potassium infusion in sepsis and septic shock: no hard evidence yet.Crit Care2003;7,13-15. [PubMed]
 
van den Berghe, G, Wouters, P, Weekers, F, et al Intensive insulin therapy in the critically ill patients.N Engl J Med2001;345,1359-1367. [CrossRef] [PubMed]
 

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References

Cely, CM, Arora, P, Quartin, AA, et al (2004) Relationship of baseline glucose homeostasis to hyperglycemia during medical critical illness.Chest126,879-887. [CrossRef] [PubMed]
 
van der Horst, IC, Ligtenberg, JJ, Bilo, HJ, et al Glucose-insulin-potassium infusion in sepsis and septic shock: no hard evidence yet.Crit Care2003;7,13-15. [PubMed]
 
van den Berghe, G, Wouters, P, Weekers, F, et al Intensive insulin therapy in the critically ill patients.N Engl J Med2001;345,1359-1367. [CrossRef] [PubMed]
 
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