Thiamine Levels During Intensive Insulin Therapy in Critically Ill Patients

2016 ◽  
Vol 32 (9) ◽  
pp. 559-564 ◽  
Author(s):  
Wouter van Snippenburg ◽  
Mariet G. J. Reijnders ◽  
Jose G. M. Hofhuis ◽  
Rien de Vos ◽  
Stephan Kamphuis ◽  
...  

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.

2009 ◽  
Vol 3 (6) ◽  
pp. 1302-1308 ◽  
Author(s):  
Moritoki Egi ◽  
Rinaldo Bellomo

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.


2007 ◽  
Vol 18 (2) ◽  
pp. 200-212
Author(s):  
Julia Lindeman Read ◽  
Eugene Y. Cheng

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.


Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 987
Author(s):  
Ahmad Aljada ◽  
Ghada Fahad AlGwaiz ◽  
Demah AlAyadhi ◽  
Emad Masuadi ◽  
Mahmoud Zahra ◽  
...  

Purpose: This study examined the effect of permissive underfeeding compared to target feeding and intensive insulin therapy (IIT) compared to conventional insulin therapy (CIT) on the inflammatory mediators monocyte chemoattractant protein 1 (MCP-1), soluble intercellular adhesion molecule 1 (sICAM-1), and tissue factor (TF) in critically ill patients. Methodology: This was a substudy of a 2 × 2 factorial design randomized controlled trial in which intensive care unit (ICU) patients were randomized into permissive underfeeding compared to target feeding groups and into IIT compared to CIT groups (ISRCTN96294863). In this substudy, we included 91 patients with almost equal numbers across randomization groups. Blood samples were collected at baseline and at days 3, 5, and 7 of an ICU stay. Linear mixed models were used to assess the differences in MCP-1, sICAM-1, and TF across randomization groups over time. Results: Baseline characteristics were balanced across randomization groups. Daily caloric intake was significantly higher in the target feeding than in the permissive underfeeding groups (P-value < 0.01), and the daily insulin dose was significantly higher in the IIT than in the CIT groups (P-value < 0.01). MCP-1, sICAM-1, and TF did not show any significant difference between the randomization groups, while there was a time effect for MCP-1. Baseline sequential organ failure assessment (SOFA) score and platelets had a significant effect on sICAM-1 (P-value < 0.01). For TF, there was a significant association with age (P-value < 0.01). Conclusions: Although it has been previously demonstrated that insulin inhibits MCP-1, sICAM-1 in critically ill patients, and TF in non-critically ill patients, our study demonstrated that IIT in critically ill patients did not affect these inflammatory mediators. Similarly, caloric intake had a negligible effect on the inflammatory mediators studied.


2010 ◽  
Vol 25 (1) ◽  
pp. 84-89 ◽  
Author(s):  
José Raimundo A. de Azevedo ◽  
Leonardo Oliveira de Araujo ◽  
Widlani Sousa da Silva ◽  
Renato Palácio de Azevedo

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