Perioperative diabetic and hyperglycemic management issues

Coursin, Douglas B.; Connery, Lisa; Ketzler, Jonathan T.

doi:10.1097/01.ccm.0000115623.52021.c0

Cited by 92 publications

(70 citation statements)

References 74 publications

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“…Diabetes complications that are debilitating include poor wound healing (2). The impaired healing affects the resolution of both acute and chronic wounds (3), which represent a significant health care burden in the U.S. As an example, ulcerations of the lower extremities, which heal poorly in diabetic patients, are a significant cause of hospitalization and are usually the first step in limb amputation (4).…”

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Diabetes Enhances mRNA Levels of Proapoptotic Genes and Caspase Activity, Which Contribute to Impaired Healing

et al. 2006

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We previously reported that after a bacteria-induced wound in the scalp, type 2 diabetic (db/db) mice had higher levels of apoptosis of fibroblasts and bone-lining cells that are critical for healing compared with normoglycemic controls. To investigate mechanisms by which this might occur, RNA profiling and caspase activity was measured after inoculation of Porphyromonas gingivalis. Diabetes caused a more than twofold induction of 71 genes that directly or indirectly regulate apoptosis and significantly enhanced caspase-8, -9, and -3 activity. The functional significance of diabetes-induced apoptosis was studied by treating diabetic mice with a pancaspase inhibitor, z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone). Inhibiting apoptosis significantly improved several parameters of healing, including fibroblast density, enhanced mRNA levels of collagen I and III, and increased matrix formation. Improvements were also noted in bone, with an increase in the number of bone-lining cells and new bone formation. Thus, diabetes-enhanced apoptosis represents an important mechanism through which healing is impaired, and this can be explained, in part, by diabetes-increased expression of proapoptotic genes and caspase activity. Diabetes 55: 487-495, 2006 D iabetes affects Ͼ18 million Americans and causes significant morbidity and mortality (1). Diabetes complications that are debilitating include poor wound healing (2). The impaired healing affects the resolution of both acute and chronic wounds (3), which represent a significant health care burden in the U.S. As an example, ulcerations of the lower extremities, which heal poorly in diabetic patients, are a significant cause of hospitalization and are usually the first step in limb amputation (4). Of the 18 million people in the U.S. with diabetes, 20% will at some point develop ulcers that heal poorly (5,6).Healing of wounds in diabetes is characterized by delays in the repair process as well as a decrease in the tensile strength of healing wounds (3,7). Deficiencies in fibroblast numbers have been reported to represent an important aspect of delayed wound healing in diabetes (8 -10). It has been suggested that aberrant growth factor expression, altered inflammatory responses, or enhanced glycosylation of proteins may be involved (8,11,12). Alternatively, enhanced apoptosis may decrease fibroblast numbers, which could contribute to impaired diabetic healing (13). Whatever the cause, the generation and maintenance of a sufficient number of fibroblasts to participate in wound repair may be particularly important in diabetes. Humans with type 1 diabetes have impaired osseous healing (14). That this may be caused by reduced bone formation is supported by findings that serum osteocalcin levels are significantly lower in type 1 diabetic patients (15), and there is a reduction in osteoblast numbers and function (16 -18). In type 2 diabetes, there is evidence of diminished bone formation, increased risk of fracture, and impaired healing, but the mechanisms are not we...

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Diabetes Enhances mRNA Levels of Proapoptotic Genes and Caspase Activity, Which Contribute to Impaired Healing

et al. 2006

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“…Patients with diabetes are affected, but patients with stress hyperglycemia with no previous diagnosis of diabetes also have a poor prognosis (1,2,7,8). Critical illness and trauma induce counterregulatory hormone release and alterations in carbohydrate metabolism such as enhanced hepatic gluconeogenesis, insulin resistance, and relative insulin deficiency (9,10).…”

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Multicentric, Randomized, Controlled Trial to Evaluate Blood Glucose Control by the Model Predictive Control Algorithm Versus Routine Glucose Management Protocols in Intensive Care Unit Patients

et al. 2006

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OBJECTIVE -To evaluate a fully automated algorithm for the establishment of tight glycemic control in critically ill patients and to compare the results with different routine glucose management protocols of three intensive care units (ICUs) across Europe (Graz, Prague, and London).RESEARCH DESIGN AND METHODS -Sixty patients undergoing cardiac surgery (age 67 Ϯ 9 years, BMI 27.7 Ϯ 4.9 kg/m 2 , 17 women) with postsurgery blood glucose levels Ͼ120 mg/dl (6.7 mmol/l) were investigated in three different ICUs (20 per center). Patients were randomized to either blood glucose management (target range 80 -110 mg/dl [4.4 -6.1 mmol/l]) by the fully automated model predictive control (MPC) algorithm (n ϭ 30, 10 per center) or implemented routine glucose management protocols (n ϭ 30, 10 per center). In all patients, arterial glucose was measured hourly to describe the glucose profile until the end of the ICU stay but for a maximum period of 48 h. CONCLUSIONS -The data suggest that the MPC algorithm is safe and effective in controlling glycemia in critically ill postsurgery patients. RESULTS Diabetes Care 29:271-276, 2006E pidemiological studies have revealed a significant relationship between impaired glycemic control and poor outcome in patients with acute cardiovascular events (1-3), postoperative wound infections (4,5), and trauma (6). Patients with diabetes are affected, but patients with stress hyperglycemia with no previous diagnosis of diabetes also have a poor prognosis (1,2,7,8). Critical illness and trauma induce counterregulatory hormone release and alterations in carbohydrate metabolism such as enhanced hepatic gluconeogenesis, insulin resistance, and relative insulin deficiency (9,10).A growing body of evidence indicates that treatment of hyperglycemia improves clinical outcome (11). In a prospective randomized trial in Leuven, postoperative patients were treated with an intensive insulin protocol (12). Strict glycemic control (80 -110 mg/dl) resulted in a reduction of in-hospital mortality and a decrease in organ system dysfunction compared with moderate hyperglycemia (180 -200 mg/dl). In another study performed on a mixed medical-surgical population, the implementation of an intensive glucose management protocol led to decreased mortality, morbidity, and length of intensive care unit (ICU) stay of critically ill adult patients (13).Based on this clinical evidence, efforts have to be made to maintain strict glycemic control in critically ill patients. To achieve this goal, the implementation of complex intensive insulin infusion protocols based on frequent bedside glucose monitoring is required. Numerous guidelines have been developed and tested to implement tight glycemic control in ICUs (13-18). However, most of these guidelines still require user interventions or intuitive decisions of ICU staff.The development of a closed-loop control system that automatically regulates the dose of insulin based on glucose measurements could permit tight glycemic control without increasing the work-

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“…The combined GIK infusion is efficient, safe and effective but does not permit selective adjustment of insulin delivery without changing the bag. Separate continuous glucose and insulin infusions are used more frequently than the glucose-potassium-insulin infusion (Coursin et al, 2004;Furnary et al, 2003;Goldberg et al, 2004;Rehman & Mohammed, 2003). A proposed regimen for separate IV insulin infusion for perioperative diabetes management is shown in …”

Section: Diabetesmentioning

confidence: 99%