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From the Departments of Intensive Care Medicine (Drs. Van den Berghe, Schoonheydt, and Becx, and P.J. Wouters) and Physical Medicine and Rehabilitation (Dr. Bruyninckx), Catholic University of Leuven, Belgium.
Address correspondence and reprint requests to Prof. Greet Van den Berghe, Department of Intensive Care Medicine, Catholic University of Leuven, B-3000 Leuven, Belgium; e-mail: greta.vandenberghe{at}med.kuleuven.ac.be
Objective: To investigate the effectiveness of maintaining blood glucose levels below 6.1 mmol/L with insulin as prevention of secondary injury to the central and peripheral nervous systems of intensive care patients.
Methods: The authors studied the effect of intensive insulin therapy on critical illness polyneuropathy (CIPNP), assessed by weekly EMG screening, and its impact on mechanical ventilation dependency, as a prospectively planned subanalysis of a large randomized, controlled trial of 1,548 intensive care patients. In the 63 patients admitted with isolated brain injury, the authors studied the impact of insulin therapy on intracranial pressure, diabetes insipidus, seizures, and long-term rehabilitation at 6 and 12 months follow-up.
Results: Intensive insulin therapy reduced ventilation dependency (p = 0.0007; Mantel–Cox log rank test) and the risk of CIPNP (p < 0.0001). The risk of CIPNP among the 405 long-stay (
7 days in intensive care unit) patients was lowered by 49% (p < 0.0001). Of all metabolic and clinical effects of insulin therapy, and corrected for known risk factors, the level of glycemic control independently explained this benefit (OR for CIPNP 1.26 [1.09 to 1.46] per mmol blood glucose, p = 0.002). In turn, prevention of CIPNP explained the ability of intensive insulin therapy to reduce the risk of prolonged mechanical ventilation (OR 3.75 [1.49 to 9.39], p = 0.005). In isolated brain injury patients, intensive insulin therapy reduced mean (p = 0.003) and maximal (p < 0.0001) intracranial pressure while identical cerebral perfusion pressures were obtained with eightfold less vasopressors (p = 0.01). Seizures (p < 0.0001) and diabetes insipidus (p = 0.06) occurred less frequently. At 12 months follow-up, more brain-injured survivors in the intensive insulin group were able to care for most of their own needs (p = 0.05).
Conclusions: Preventing even moderate hyperglycemia with insulin during intensive care protected the central and peripheral nervous systems, with clinical consequences such as shortening of intensive care dependency and possibly better long-term rehabilitation.
Editorial, see page 1330
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the April 26 issue to find the title link for this article.
Supported by the Fund for Scientific Research, Flanders, Belgium (G.0278.03), the Research Council of the Catholic University of Leuven (OT 03/56), and the Belgian Foundation for Research in Congenital Heart Diseases. G.V.d.B. is a Fundamental Clinical Research Investigator (G.3C05.95N) for the Fund for Scientific Research, Flanders. G.V.d.B. holds an unrestrictive Catholic University of Leuven Novo Nordisk Chair of Research.
Presented in part at the 16th annual congress of the European Society of Intensive Care Medicine; October 5–8, 2003; Amsterdam, Netherlands; and at the 86th annual meeting of the Endocrine Society; June 16–19, 2004; New Orleans, LA.
Received June 14, 2004. Accepted in final form December 22, 2004.
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