Intensive Insulin Therapy for Acute Hyperglycemia

There is growing evidence that control of hyperglycemia in the critically ill patient improves outcome. Normalizing blood glucose levels decreases the risk of developing sepsis, end-organ damage, and hospital mortality. Critical care clinicians must be familiar with current and benchmark research supporting control of hyperglycemia and use this knowledge to ensure appropriate application of evidence-based practice for decreasing or preventing complications in the critically ill patient. This article describes the effects of hyperglycemia and discusses the evidence supporting tight glycemic control in such patients. The necessary steps to implement an intensive insulin therapy protocol for control of acute hyperglycemia are detailed.

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Regulation of the Somatotropic Axis by Intensive Insulin Therapy during Protracted Critical Illness

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2003-032102 ◽

2004 ◽

Vol 89 (7) ◽

pp. 3105-3113 ◽

Cited By ~ 39

Author(s):

Dieter Mesotten ◽

Pieter J. Wouters ◽

Robin P. Peeters ◽

Kevin V. Hardman ◽

Jeff M. Holly ◽

...

Keyword(s):

Blood Glucose ◽

Critical Illness ◽

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Somatotropic Axis ◽

Glucose Levels ◽

Blood Glucose Levels ◽

Igf I ◽

Serum Gh

Abstract The catabolic state of critical illness has been linked to the suppressed somatotropic GH-IGF-binding protein (IGFBP) axis. In critically ill patients it has been demonstrated that, compared with the conventional approach, which only recommended insulin therapy when blood glucose levels exceeded 12 mmol/liter, strict maintenance of blood glucose levels below 6.1 mmol/liter with intensive insulin therapy almost halved intensive care mortality, acute renal failure, critical illness polyneuropathy, and bloodstream infections. Poor blood glucose control in diabetes mellitus has also been associated with low serum IGF-I levels, which can be increased by insulin therapy. We hypothesized that intensive insulin therapy would improve the IGF-I axis, possibly contributing to the clinical correlates of anabolism. Therefore, this study of 363 patients, requiring intensive care for more than 7 d and randomly assigned to either conventional or intensive insulin therapy, examines the effects of intensive insulin therapy on the somatotropic axis. Contrary to expectation, intensive insulin therapy suppressed serum IGF-I, IGFBP-3, and acid-labile subunit concentrations. This effect was independent of survival of the critically ill patient. Concomitantly, serum GH levels were increased by intensive insulin therapy. The suppression of IGF-I in association with the increased GH levels suggests GH resistance induced by intensive insulin therapy, which was reflected by the decreased serum GH-binding protein levels. Intensive insulin therapy did not affect IGFBP-3 proteolysis, which was markedly higher in protracted critically ill patients compared with healthy controls. Also, intensive insulin therapy did not suppress the urea/creatinine ratio, a clinical correlate of catabolism. In conclusion, our data suggest that intensive insulin therapy surprisingly suppressed the somatotropic axis despite its beneficial effects on patient outcome. GH resistance accompanied this suppression of the IGF-I axis. To what extent and through which mechanisms the changes in the GH-IGF-IGFBP axis contributed to the survival benefit under intensive insulin therapy remain elusive.

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Intensive Insulin Therapy and Pentastarch Resuscitation in Sepsis

50 Studies Every Anesthesiologist Should Know ◽

10.1093/med/9780190237691.003.0021 ◽

2018 ◽

pp. 109-113

Keyword(s):

Septic Shock ◽

Severe Sepsis ◽

Blood Glucose ◽

Insulin Therapy ◽

Fluid Resuscitation ◽

Intensive Insulin Therapy ◽

Safety And Efficacy ◽

Glucose Levels ◽

Blood Glucose Levels ◽

Ringer’S Lactate

This case focuses on the use of intensive insulin therapy with sepsis by asking the question: What are the safety and efficacy of intensive insulin therapy compared with conventional therapy and hydroxyethyl starch (HES) compared with Ringer’s lactate in patients with severe sepsis or septic shock? This study demonstrated that critically ill patients did not benefit from intensive insulin therapy targeting blood glucose levels of 80–110 mg/dL vs. conventional insulin therapy nor from fluid resuscitation with HES vs. Ringer’s lactate. Neither intensive insulin therapy nor fluid resuscitation with HES is currently recommended in major sepsis guidelines.

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Thiamine Levels During Intensive Insulin Therapy in Critically Ill Patients

Journal of Intensive Care Medicine ◽

10.1177/0885066616659429 ◽

2016 ◽

Vol 32 (9) ◽

pp. 559-564 ◽

Cited By ~ 5

Author(s):

Wouter van Snippenburg ◽

Mariet G. J. Reijnders ◽

Jose G. M. Hofhuis ◽

Rien de Vos ◽

Stephan Kamphuis ◽

...

Keyword(s):

Insulin Therapy ◽

Critically Ill ◽

Intensive Insulin Therapy ◽

Critically Ill Patients ◽

Thiamine Deficiency ◽

Gastrointestinal Disease ◽

Glucose Levels ◽

Gastrointestinal Pathology ◽

Observational Prospective Cohort Study ◽

Thiamine Level

Introduction: Thiamine is an essential cofactor in carbohydrate metabolism, and deficiency can therefore cause various organ dysfunctions. Little is known about the prevalence and possible worsening of thiamine deficiency in critically ill patients. In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores. Materials and Methods: An observational prospective cohort study was carried out in a medical–surgical ICU in a general teaching hospital in Apeldoorn, the Netherlands. All adults who were treated during that time with intensive insulin therapy were included. Deficiency was defined as a thiamine level <100 nmol/L. No thiamine supplementation was administered except for normal amounts present in standard enteral feeding. Results: A total of 58 patients were available for analysis. Median thiamine level at admission was 111 nmol/L. Deficiency was present in 39.7% of patients and was significantly associated with the presence of gastrointestinal pathology and with recent surgery. Thiamine levels increased a median of 14 nmol/L in 48 hours. Only 3.4% of patients showed a predefined relevant decline in thiamine levels. Conclusion: Intensive insulin therapy does not appear to cause or worsen thiamine deficiency. However, based on the high prevalence of deficiency at admission, it might be warranted to supplement thiamine in all patients admitted to the ICU, especially when there is an underlying gastrointestinal disease or recent surgery.

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Reducing Glycemic Variability in Intensive Care Unit Patients: A New Therapeutic Target?

Journal of Diabetes Science and Technology ◽

10.1177/193229680900300610 ◽

2009 ◽

Vol 3 (6) ◽

pp. 1302-1308 ◽

Cited By ~ 31

Author(s):

Moritoki Egi ◽

Rinaldo Bellomo

Keyword(s):

Intensive Care Unit ◽

Intensive Care ◽

Insulin Therapy ◽

Critically Ill ◽

Patient Outcomes ◽

Intensive Insulin Therapy ◽

Critically Ill Patients ◽

Glycemic Variability ◽

Glucose Levels ◽

Lower Glucose

Acute hyperglycemia is common in critically ill patients. Strict control of blood glucose (BG) concentration has been considered important because hyperglycemia is associated independently with increased intensive care unit mortality. After intensive insulin therapy was reported to reduce mortality in selected surgical critically ill patients, lowering of BG levels was recommended as a means of improving patient outcomes. However, a large multicenter multination study has found that intensive insulin therapy increased mortality significantly. A difference in variability of BG control may be one possible explanation why the effect of intensive insulin therapy varied from beneficial to harmful. Several studies have confirmed significant associations between variability of BG levels and patient outcomes. Decreasing the variability of the BG concentration may be an important dimension of glucose management. If reducing swings in the BG concentration is a major biologic mechanism behind the putative benefits of glucose control, it may not be necessary to pursue lower glucose levels with their attendant risk of hypoglycemia.

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