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Performance improvement measures in achieving glycemic control in the acute brain injury population.(CE)(Report)


ABSTRACT

Glycemic control is becoming a standard practice in the intensive care environment because it has been shown to produce positive patient outcomes and benefits. A 14-bed neurointensive care unit initiated a strict glycemic protocol and evaluated the results over a 1-year period through a performance improvement initiative. Results indicated that tight glycemic control could be achieved safely by adhering to an evidence-based established protocol. The average blood glucose level for all patients was between 90 and 130 mg/dl by Day 2 after the implementation of the glycemic control protocol. The purpose of this article was to explain how a strict glycemic protocol was safely implemented. Further research is necessary to determine long-term benefits of glycemic control in the population with neurocritical illness.

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Glycemic control has become a growing trend in inpatient treatment and clinical research. Hyperglycemia has been identified as a frequent concurrent diagnosis in those with critical illness, even for those without a past medical history significant for diabetes mellitus. More often, hyperglycemia is being recognized as an independent risk factor potentially leading to further complications in both surgical and medical patient populations (Ellger et al., 2006). This phenomenon has evolved into a significant issue among the critical brain injury population, despite the patient's age, gender, race, past medical history, and state of health before injury. Research has shown that early intervention in glycemic control improves clinical outcome in the population with critical illness in both medically and surgically treated patients by reducing morbidity and mortality rates, infection rates, critical illness polyneuropathy, myopathy, the amount of time spent on mechanical ventilation, myocardial dysfunction, seizures, impaired recovery of organ failure, and neuromuscular dysfunction while improving wound healing (Ellger et al., 2006; Gearhart & Parbhoo, 2006; Hermans et al., 2007; Presutti & Millo, 2006).

Hepatic and peripheral insulin resistance and related insulin deficiency caused by a minute compensatory mechanism of pancreatic B cells have been shown to cause hyperglycemia in the population with critical illness, independent of the underlying disease process (Ellger et al., 2006). Glucose has been associated with brain tissue acidosis in patients who have experienced a major head injury (Zygun et al., 2004). Conditions such as diuresis, dehydration, ketonemia, electrolyte imbalance, and changes in mental status have been associated with acute hyperglycemia. Impaired immune responses to injuries and infections, impaired gastrointestinal motility, high cardiovascular tonus, impaired wound healing, and higher mortality rates are some of the pathologies that have been reported as consequences of hyperglycemia (Khoury, Klausner, Ben-Abraham, & Szold, 2004).

Furthermore, in patients who have sustained a traumatic brain injury, transient hyperglycemia has been shown to adversely affect cerebral energy metabolism when the blood glucose level is greater than 15 mmol/L. This increase is associated with a moderate increase in cerebral lactate levels (Diaz-Parejo et al., 2003). Diaz-Parejo et al. (2003) reported that transient moderate hyperglycemia did not in fact affect cerebral energy metabolism, as defined by a blood glucose concentration of 12 to 15 mmol/L. Acute or new hyperglycemia has been believed to occur in 5% to 30% of patients with critical illness due to the hormonal response to stress (Khoury et al., 2004).

This article describes the implementation of a glycemic control protocol, predicted upon evidenced-based research in a 14-bed neuroscience trauma surgical intensive care unit (NTSICU). The protocol was designed specifically for neurocritical care patients. The patient population cared for in the 14-bed NTSICU consisted of patients with various neurological diseases, traumatic brain injuries, subarachnoid hemorrhages, cerebral aneurysms, traumatic spinal cord injuries, strokes, brain tumors, and neurosurgical procedures, both emergent and planned. The patient population consisted of a mixed medical-surgical care environment. After a time allotted for data collection, an advanced practice nurse (APN) evaluated the performance of the staffs adherence to the newly developed glycemic control protocol. Implications for practice and recommendations for further research are discussed as well.

Literature Review

Taylor et al. (2006) concluded that a nurse-driven protocol for glycemic control led to more effective outcomes compared with a physician-managed protocol in the surgical intensive care environment. Results of their study demonstrated that more effective outcomes could be achieved by a nurse-driven glycemic protocol without a major increase in hypoglycemia; however, the tighter glycemic control protocol led to a lengthier time spent on an insulin infusion.

Because of a landmark study conducted by Van den Berghe et al. (2001), the positive benefits of intensive insulin therapy in the patient population with critical illness were clearly defined. Van den Berghe et al. performed a large prospective, randomized, controlled trial at a single institution. The researchers theorized that hyperglycemia and/or relative insulin deficiency contributed to a cascade of negative complications for surgical intensive care patients. A total of 1,548 participants were enrolled in the study over a 12-month time period. Patients qualified for enrollment into the study if they were being treated in the intensive care unit and were receiving mechanical ventilation. Upon admission, these patients were randomly assigned to receive either conventional or intensive insulin therapy. A continuous insulin infusion was initiated within the conventional group when the blood glucose level surpassed 215 mg/dl. The infusion was then regulated to maintain a blood glucose level between 180 and 200 mg/dl. The intervention group had tighter glucose parameters, and their infusions began when blood glucose levels went above 110 mg/dl and then were maintained to sustain a blood glucose level between 80 and 110 mg/dl. Whole blood glucose levels, either obtained from an arterial line or a capillary, were monitored every 1 to 4 hours, and the insulin infusion rate was adjusted and maintained by intensive care nurses according to a strict glycemic algorithm. According to the study protocol, the maximum insulin rate was set at 50 units per hour.

Results indicated a 4.6% mortality rate of patients in the intensive insulin therapy versus an 8% mortality rate in the conventional group. Mortality was reduced by 34% in the intensive insulin therapy group. The greatest reduction in mortality was attributed to the reduction in deaths related to multisystem organ failure with a confirmed septic focus. Those patients who were hospitalized in the intensive care unit for greater than 5 days seemed to benefit the most from the intensive insulin therapy. Multiple other advantages of intensive insulin therapy were identified through this groundbreaking trial. The intensive insulin therapy group inpatient mortality was reduced by 34%, blood stream infections were reduced by 46%, acute renal failure requiring dialysis or hemofiltration was reduced by 41%, the median number of red cell infusions was reduced by 50%, critical illness polyneuropathy was reduced by 44%, and the rate of prolonged mechanical ventilation was less likely to occur in those treated with the intensive insulin therapy.

In the study conducted by Van den Berghe et al. (2001), the benefits of normoglycemia were inferred from the research conducted in the surgical intensive care unit. Recommendations were to research the benefits of normoglycemia in the medical intensive care setting as well. Van den Berghe, Wilmer, Hermans, et al. (2006) conducted another randomized controlled study at the same single-center site where 1,200 patients were randomly assigned to either a conventional or an intensive insulin therapy group in the medical intensive care unit. The study design and methods of data collection were the same as those described in the research study of Van den Berghe et al. (2001). Results indicated that inpatient mortality was not reduced in the intensive insulin therapy group, but blood glucose level was lowered. Yet, the reduction of newly acquired kidney injury, the accelerated weaning from mechanical ventilation, and the accelerated discharge from the intensive care unit and the hospital in general were achieved in the group randomized into receiving the intensive insulin therapy. The length of stay in the intensive care unit related to insulin therapy did not correlate. Those treated with intensive insulin therapy who stayed in the intensive care unit less than 3 days had a higher mortality rate versus that of the conventional therapy group. When the length of stay in the intensive care unit was greater than 3 days, inpatient mortality was reduced dramatically from 52.5% to 43% (p = 0.009). The significance of this study is related to the benefits of reduction of morbidity versus that of mortality for those who received intensive insulin therapy.

Achieving euglycemia without becoming hypoglycemic has been the challenge to most clinical research studies. Van den Berghe, Wilmer, Milants, et al. (2006) performed an analysis of two randomized clinical research trials, those of Van den Berghe et al. (2001) and Van den Berghe, Wilmer, Hermans, et al. (2006), that evaluated and compared effective glucose control in both medical and surgical intensive care units. Van den Berghe, Wilmer, Milants, et al. (2006) established an acceptable glucose level for patients being treated in both medical and surgical intensive care units. Upon evaluation of all of the data, the researchers concluded that the optimal target glucose of less than 110 mg/dl was more beneficial than was the range of 110-150 mg/dl. However, the target glucose of less than 110 mg/dl also carried the greatest risk for hypoglycemia (10.7%) versus that of the 110-150 mg/dl range (4.3%) and greater than 150 mg/dl (2.9%). Within the conventional therapy group, hypoglycemia defined as a blood glucose level less than or equal to 40 mg/dl occurred in 1.8% of patients and in 11.3% of patients randomized to the intensive insulin therapy group (p < .0001). Patients who received more caloric intake had a higher occurrence of hypoglycemia than those who received fewer calories. Hypoglycemia was not found to have been responsible for any early deaths, rather abrupt and temporary morbidity in a small number of patients. Among the patients with documented hypoglycemia, immediate symptoms occurred in 5% of patients studied. Immediate consequences related to hypoglycemia were considered to be sweating, hemodynamic collapse, arrhythmia, decreased consciousness, epilepsy, or coma within 8 hours. Potential late sequelae of hypoglycemia included altered neurological status, epilepsy, coma, or death before hospital discharge. Three patients in the conventional therapy group and six patients in the intensive insulin therapy group displayed immediate transient symptoms of hypoglycemia, all of which fully recovered within 8 hours. There were also no permanent neurological sequelae among hospital survivors related to hypoglycemia from the intensive insulin therapy. Deaths that occurred within 24 hours of the first hypoglycemic event included three patients (12%) in the conventional therapy group and one patient (0.6%) in the intensive insulin therapy group. Overall, hospital mortality among patients who experienced a hypoglycemic event was similar in the conventional (52%) and intensive insulin therapy (50.6%) groups. According to Van den Berghe, Wilmer, Milants, et al. (2006), intensive insulin therapy causes minimal harm and reduces morbidity and mortality mutually in medical and surgical intensive unit patients. Despite these results, research from this study inferred that patients with diabetes did not significantly benefit from the intensive insulin therapy.

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COPYRIGHT 2009 American Association of Neuroscience Nurses Reproduced with permission of the copyright holder. Further reproduction or distribution is prohibited without permission.

Copyright 2009 Gale, Cengage Learning. All rights reserved. Gale Group is a Thomson Corporation Company.

NOTE: All illustrations and photos have been removed from this article.


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