Stress-hyperglycemia, insulin and immunomodulation in sepsis.
Stress-hyperglycemia and insulin resistance are exceedingly common in critically ill patients, particularly those with sepsis. Multiple pathogenetic mechanisms are responsible for this metabolic syndrome; however, increased release of pro-inflammatory mediators and counter-regulatory hormones may play a pivotal role. Recent data suggests that hyperglycemia may potentiate the pro-inflammatory response while insulin has the opposite effect. Furthermore, emerging evidence suggests that tight glycemic control will improve the outcome of critically ill patients. This paper reviews the pathophysiology of stress hyperglycemia in the critically ill septic patient and outlines a treatment strategy for the management of this disorder.
Department of Critical Care Medicine, University of Pittsburgh Medical Center, 640A Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261, USA. maripe@ccm.upmc.edu
Paul E
PE
Marik
Murugan
M
Raghavan
D003422:Critical Care; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D006943:Hyperglycemia / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D007328:Insulin / Q000276:immunology / Q000627:therapeutic use*; D007333:Insulin Resistance; D018805:Sepsis / Q000276:immunology / Q000401:mortality / Q000503:physiopathology*; D013312:Stress, Physiological / Q000150:complications / Q000378:metabolism*
D007328:Insulin; D005947:Glucose; D006854:Hydrocortisone