Clinical paperStrict normoglycaemic blood glucose levels in the therapeutic management of patients within 12 h after cardiac arrest might not be necessary☆
Introduction
Sudden cardiac death is a major clinical and public health problem1 and the long-term prognosis of cardiac arrest survivors is still poor.2, 3 Only about one third of all patients admitted to a hospital after cardiac arrest can be discharged.4 Two third of the patients dying after admission die from neurological injury.5
Prediction of survival and neurological outcome remains difficult, especially in the first 48 h after cardiac arrest.6 High blood glucose on admission has been shown to be associated with adverse outcome and mortality in patients with cardiac arrest, myocardial infarction and stroke.7, 8, 9, 10, 11, 12 In cardiac arrest patients, this admission blood glucose has also been considered to be a surrogate for a long interval to restoration of spontaneous circulation.
Since the studies of Van den Berghe,13, 14 blood glucose control has become an important issue in the treatment of critical ill patients. And therefore the new guidelines for cardiopulmonary resuscitation,15 recommend monitoring blood glucose frequently and treat hyperglycaemia in patients after cardiac arrest. But the optimum blood glucose target has not yet been determined.
In this study we aim to validate the relationship between blood glucose values 12 h after restoration of spontaneous circulation and survival with good neurological recovery to see, if strict normoglycaemia is necessary within this time. In addition the association of blood glucose levels in the application of “mild therapeutic hypothermia” and “no-flow” times (time interval from collapse to cardiopulmonary resuscitation), “low-flow” times (time interval of cardiopulmonary resuscitation) and the dose of adrenaline (epinephrine) used during resuscitation was investigated.
Section snippets
Materials and methods
The data set of the prospective randomised European multicentre trial on mild therapeutic hypothermia to improve neurological outcome after cardiac arrest16 has been analysed retrospectively. The work was approved by the appropriate ethical committees related to the institutions in which it was performed.
Patients aged 18–75 years in whom spontaneous circulation had been restored after witnessed cardiac arrest due to ventricular fibrillation or non-perfusing ventricular tachycardia were assigned
Results
Between March 1996 and January 2001, 275 patients were enrolled into the hypothermia after cardiac arrest trial. In exploratory analyses we found an interaction between a known history of diabetes mellitus and the effect of glucose levels on neurological outcome. Since the small number of diabetic patients did not allow a separate analysis, all patients with a known history of diabetes (n = 37) were excluded. Furthermore, four patients were excluded because information on diabetes was missing.
Discussion
This retrospective analysis of data obtained from a previous randomised clinical trial about the effect of mild hypothermia after cardiac arrest on survival and neurological recovery16 demonstrates that moderate elevation of blood glucose at 12 h after cardiac arrest is associated with good outcome. Survival and good neurological recovery showed to be better independently from all confounders such as “no-flow” and “low-flow” time or epinephrine dose administered during cardiopulmonary
Conclusion
Blood glucose levels 12 h after return of spontaneous circulation are predictive not only for survival but also for neurological outcome, independently from no-flow, low-flow time and epinephrine dosage. Near normoglycaemic blood glucose levels (67–115 mg/dl; 3.72–6.38 mmol/l) were not associated with better neurological outcome than a blood glucose level of 116–143 mg/dl (6.44–7.94 mmol/l), which has an important therapeutic implication. Further prospective studies are necessary to determine the
Conflict of interest
There is no conflict of interest.
Funding source
Supported by grants from BIOMED2 European Commission, DG XII for Science Research and Development, Directorate Life Science and Technologies, Biomedical and Health Research Division (BMH4-CD-96-0667); Ministry of Science and Transport, Austria (GZ 5.550/12-Pr/4/95, GZ 650.0251/2-IV/6/96); and Austrian Science Foundation (P11405-MED).
Acknowledgments
We are indebted to the Hypothermia After Cardiac Arrest (HACA) Study Group investigators [A. Zeiner (Universitätsklinik für Notfallmedizin, Vienna, Austria; 88 patients); A. Valentin (Krankenhaus Rudolfstiftung, Vienna, Austria; 2 patients); M. De Meyer (A.Z. Sint Jan, Bruges, Belgium; 35 patients); O. Takkunen (Helsingin yliopistollinen keskussairaala, Helsinki, Finland; 71 patients); S. Hachimi-Idrissi, L. Huyghens (Academisch Ziekenhuis van de Vrije Universiteit Brussel, Brussels, Belgium;
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A Spanish translated version of the summary of this article appears as Appendix in the final online version at 10.1016/j.resuscitation.2007.08.003.