Insulin Infusion Protocols for critically ill Patients: a Highlight of Differences and Similarities

Western University of Health Sciences, Pomona, California 91766-1854, USA.
Endocrine Practice (Impact Factor: 2.81). 03/2007; 13(2):137-46. DOI: 10.4158/EP.13.2.137
Source: PubMed


To discuss the major differences and similarities among the currently published insulin infusion protocols (IIPs) for critically ill patients.
IIPs were identified by searching MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials. The reference lists for all retrieved protocols were also reviewed to identify any IIPs that were not surfaced with use of our initial search strategies. The major differences and similarities among the IIPs were identified and examined. In addition, strategies for successful implementation of IIPs were outlined.
Our search strategies retrieved 17 IIPs. Currently, no published studies have compared one insulin protocol with another. The major differences or similarities among the published IIPs were in the following areas: patient characteristics, target glucose level, time to achieve target glucose level, incidence of hypoglycemia, rationale for adjusting the rates of insulin infusion, and methods of blood glucose measurements. Because of variations in the definition of hypoglycemia, methods of blood glucose measurement, and types of blood samples used, some comparisons across the protocols were difficult. Use of a multidisciplinary team and gaining administrative support are crucial for addressing issues and provision of necessary resources for implementing a protocol for "tight" glycemic control in critically ill patients.
Clinicians should evaluate the type of patients in their critical care units, the mean baseline glucose levels, and the available resources to determine the most appropriate and practical IIP for their institution.

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    • "One reason for this dilemma might be that intravenous (IV) insulin protocols have been designed to lower BG in order to achieve a 'normal' or 'optimal' BG target range, without consideration for their tendency to cause hypoglycemia. Indeed, the literature on manual and computerized protocols reports wide variation in performance in terms of patients reaching target and hypoglycemia rates varying from 4.6% to over 25.0% [17-20]. Moreover, the variety of methods used to measure BG (and their relative accuracy), and the metrics used to define and report hypoglycemia make it challenging to ascertain the actual risk of hypoglycemia with any degree of certainty [21]. "
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    ABSTRACT: Control of blood glucose (BG) in critically ill patients is considered important, but is difficult to achieve, and often associated with increased risk of hypoglycemia. We examined the use of a computerized insulin dosing algorithm to manage hyperglycemia with particular attention to frequency and conditions surrounding hypoglycemic events. This is a retrospective analysis of adult patients with hyperglycemia receiving intravenous (IV) insulin therapy from March 2006 to December 2007 in the intensive care units of 2 tertiary care teaching hospitals. Patients placed on a glycemic control protocol using the Clarian GlucoStabilizer IV insulin dosing calculator with a target range of 4.4-6.1 mmol/L were analyzed. Metrics included time to target, time in target, mean blood glucose +/- standard deviation, % measures in hypoglycemic ranges <3.9 mmol/L, per-patient hypoglycemia, and BG testing interval. 4,588 ICU patients were treated with the GlucoStabilizer to a BG target range of 4.4-6.1 mmol/L. We observed 254 severe hypoglycemia episodes (BG <2.2 mmol/L) in 195 patients, representing 0.1% of all measurements, and in 4.25% of patients or 0.6 episodes per 1000 hours on insulin infusion. The most common contributing cause for hypoglycemia was measurement delay (n = 170, 66.9%). The median (interquartile range) time to achieve the target range was 5.9 (3.8 - 8.9) hours. Nearly all (97.5%) of patients achieved target and remained in target 73.4% of the time. The mean BG (+/- SD) after achieving target was 5.4 (+/- 0.52) mmol/L. Targeted blood glucose levels were achieved at similar rates with low incidence of severe hypoglycemia in patients with and without diabetes, sepsis, renal, and cardiovascular disease. Glycemic control to a lower glucose target range can be achieved using a computerized insulin dosing protocol. With particular attention to timely measurement and adjustment of insulin doses the risk of hypoglycemia experienced can be minimized.
    Full-text · Article · Oct 2009 · Critical care (London, England)
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    • "To our knowledge this is the first review dedicated exclusively to quality indicators for TGC in critically ill patients. Existing reviews on TGC have focused on its effects [7,37]; evidence of its utility and its advantages were reported, and ways to implement TGC protocols successfully discussed. "
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    ABSTRACT: The objectives of this study were to systematically identify and summarize quality indicators of tight glycaemic control in critically ill patients, and to inspect the applicability of their definitions. We searched in MEDLINE for all studies evaluating a tight glycaemic control protocol and/or quality of glucose control that reported original data from a clinical trial or observational study on critically ill adult patients. Forty-nine studies met the inclusion criteria; 30 different indicators were extracted and categorized into four nonorthogonal categories: blood glucose zones (for example, 'hypoglycaemia'); blood glucose levels (for example, 'mean blood glucose level'); time intervals (for example, 'time to occurrence of an event'); and protocol characteristics (for example, 'blood glucose sampling frequency'). Hypoglycaemia-related indicators were used in 43 out of 49 studies, acting as a proxy for safety, but they employed many different definitions. Blood glucose level summaries were used in 41 out of 49 studies, reported as means and/or medians during the study period or at a certain time point (for example, the morning blood glucose level or blood glucose level upon starting insulin therapy). Time spent in the predefined blood glucose level range, time needed to reach the defined blood glucose level target, hyperglycaemia-related indicators and protocol-related indicators were other frequently used indicators. Most indicators differ in their definitions even when they are meant to measure the same underlying concept. More importantly, many definitions are not precise, prohibiting their applicability and hence the reproducibility and comparability of research results. An unambiguous indicator reference subset is necessary. The result of this systematic review can be used as a starting point from which to develop a standard list of well defined indicators that are associated with clinical outcomes or that concur with clinicians' subjective views on the quality of the regulatory process.
    Full-text · Article · Dec 2008 · Critical care (London, England)
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    • "Markers of inflammation were found to be less frequently abnormal in the intensive insulin treatment group than in the conventional treatment group (Ellger et al., 2006; Langley and Adams, 2007). Although a number of outstanding issues remain to be addressed with this concept, and the degree of benefit that normalization of circulating glucose offers may be different in different groups of patients (Preiser and Devos, 2007; Vanhorebeek et al., 2007; Nazer et al., 2007), intensive glucose control emerges as a potential therapeutic tool for critically ill patients. "
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    ABSTRACT: In critically ill patients various conditions may lead to the activation of poly(ADP-ribose) polymerase (PARP). By promoting cellular energetic dysfunction, and by enhancing pro-inflammatory gene expression, PARP activation significantly contributes to the pathogenesis of shock. PARP activation is usually triggered by DNA strand breakage, which is typically the result of the overproduction of various reactive oxidant species. One of the pathophysiological conditions associated with PARP activation is hyperglycemia, where the reactive species are produced from the mitochondria and other cellular sources. In the present study we tested whether endotoxin-induced PARP activation and pro-inflammatory mediator production can be modified by insulin therapy. Rats subjected to bacterial lipopolysaccharide (LPS) with or without insulin co-treatment were studied. LPS-induced PARP activation in circulating lymphocytes was measured by flow cytometry, tumor necrosis factor alpha (TNF-alpha) production was measured by ELISA. The direct effect of insulin on the PARP activity of mononuclear leukocytes and human umbilical vein endothelial cells (HUVEC) in elevated glucose conditions was tested in vitro. LPS-induced significant hyperglycemic response activated PARP in circulating lymphocytes and induced TNF-alpha production. Insulin treatment prevented LPS-induced hyperglycemic response, blocked PARP activation and blunted LPS-induced TNF-alpha response. Insulin treatment caused a slight reduction in the PARP activity of mononuclear cells and HUVECs in vitro. We demonstrate that insulin treatment blocks LPS-induced PARP activation in vivo. We propose that this effect is mainly indirect, and occurs due to the prevention of stress induced hyperglycemia, with a direct cellular effect of insulin playing a potential minor supplemental role. The current findings may have significant implications in the context of the emerging concept of tight glycemic control and insulin treatment for critically ill patients.
    Full-text · Article · Feb 2008 · Life Sciences
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