The Role of Insulin and Blood Glucose Control

Abstract

Hyperglycemia in critically ill patients is a result of an altered glucose metabolism. Apart from the upregulated glucose
production (both gluconeogenesis and glycogenolysis), glucose uptake mechanisms are also affected during critical illness
and contribute to the development of hyperglycemia. The higher levels of insulin, impaired peripheral glucoseuptake and elevated
hepatic glucose production reflect the development of insulin resistance during critical illness.

Hyperglycemia in critically ill patients has been associated with increased mortality. Simply maintaining normoglycemia with
insulin therapy improves survival and reduces morbidity in surgical and medical ICU patients, as shown by two large, randomized
controlled studies. These results obtained from clinical studies were also confirmed in ‘real-life’ intensive care of a heterogeneous
patient population admitted to a mixed medical/surgical ICU.

Prevention of glucose toxicity by strict glycemic control appears to be crucial, although other metabolic and non-metabolic
effects of insulin, independent of glycemic control, may contribute to the clinical benefits.

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44
Update in Intensive Care
and Emergency Medicine
Edited by J.-L. Vincent

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E. Abraham M. Singer (Eds.)
Mechanismsof
Sepsis-InducedOrgan
DysfunctionandRecovery
With 48 Figures and 22 Tables
123

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Series Editor
Prof. Jean-Louis Vincent
Head, Department of Intensive Care
Erasme University Hospital
Route de Lennik 808, 1070 Brussels
Belgium
jlvincen@ulb.ac.be
Volume Editors
Edward Abraham, MD
University of Colorado
Health Sciences Center
Division Pulmonary & Critical Care
Medicine
E. Ninth Avenue 4200
80262 Denver, CO
USA
Mervyn Singer, MD
University College Hospital
Bloomsbury Institute of Intensive
Care
Division Medicine
Gower Street, WC1E 6BT
London
United Kingdom
ISSN 0933-6788
ISBN-10 3-540-30157-7 Springer Berlin Heidelberg New York
ISBN-13 978-3-540-30157-8 Springer Berlin Heidelberg New York
Library of Congress Control Number: 2006929196
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TableofContents
Setting the Scene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J.L. Vincent
1
TheInflammatoryResponse
Genetics and Severe Sepsis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J. Texereau, V. Lemiale, J.-P. Mira
17
Cell Signaling Pathways of the Innate Immune System
During Acute Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
S.M. Opal, P.A. Cristofaro
35
Early-Onset Pro-inflammatory Cytokines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
C. Kaech, T. Calandra
55
The Significance of HMGB1, a Late-Acting Pro-inflammatory Cytokine . . . .
E. Abraham
67
Nitric Oxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J. Carré, M. Singer, S. Moncada
77
Involvement of Reactive Oxygen and Nitrogen Species
in the Pathogenesis of Acute Lung Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
S. Matalon, I.C. Davis, J.D. Lang Jr
97
Heat Shock Proteins in Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
Z. Bromberg, Y.G. Weiss, C.S. Deutschman
Fibrosis in the Acute Respiratory Distress Syndrome. . . . . . . . . . . . . . . . . . . . . 123
D.C.J. Howell, R.C. Chambers, G.J. Laurent
Resolution of Inflammation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
G. Bellingan