Submitted by Lenore Hernandez RN, MSN, CDE, APRN-BCADM, CNS
Controlling inpatient blood sugars is challenging and complex. Inpatient blood sugars can be affected by a multitude a variables. Some of the variables are nutritional intake, inflammation, stress and steroids. Research indicates more than 50% of Americans could have diabetes or pre-diabetes by the year 2020. Healthcare costs for this population both inpatient and outpatient is enormous and growing. Many of these patients will require hospitalization. Inpatient diabetes treatment can be complex but the outcome enhancement is great. Improving inpatient blood sugar control decreases both complications and mortality. Controlling the blood sugars of this growing patient population is well worth the investment of time and resources.
Basics on Inpatient Blood Sugar Control
According to the United Health Group’s Center for Health Reform and Modernization, more than 50 percent of Americans could have diabetes or pre-diabetes by 2020 at a cost of $3.35 trillion over the next decade. Diabetes currently affects about 27 million Americans and is one of the fastest growing diseases in the nation. Another 67 million Americans are estimated to have pre-diabetes (United Health – Center for Health Reform and Modernization, 2010).
Patients with diabetes have a three-fold greater chance of hospitalization compared to those without diabetes (Smiley & Umpierrez, 2010). It is estimated that diabetes is present in 12.4-25% of hospitalized adults (Moghissi, 2010). Inpatient diabetes care is costly and is estimated to be $58 billion dollars per year (Moghissi, 2010). Concurrent with the increasing prevalence of diabetes in the United States population from 1980 through 2003, the number of patients discharged with diabetes has more than doubled, going from 2.2 to 5.1 million (Bratihwaite, et al, 2008). Controlling inpatient blood sugars can often be challenging. Blood sugar control in the hospital is essential for preventing hospital related complications. Monghissi (2010), indicates glycemic control in the hospital setting is not only a quality-of-care issue; it is a also a patient safety issue, a length-of-stay issue and a cost issue. Several retrospective analyses have shown an association between blood glucose level and hospital mortality (Braithwaithe, et al, 2008). Evidence based studies indicate reducing blood glucose levels to less than 200 reduces the risk for in hospital mortality. Length of hospital stay is also lower for patient’s whose blood sugars were controlled at 150 or less.
American Diabetes Association Guidelines (2012), American College of Physicians (2011)and The Endocrine Society (2011) all suggest a blood sugar target range of 144-180. This blood sugar range is based on the results from the Normoglycemia in Intensive Care Evaluation – Survival Using Glucose Algorithm Regulation (NICE-SUGAR) Study. The NICE-SUGAR study was published in the New England Journal of Medicine in March, 2009 and reported on the mortality in 6000 critically ill hyperglycemic patients. These patients were randomly selected to a group for tight control of blood sugar (80-108) or a group with looser control of blood sugar (144-180). Mortality for these patients had been 10% higher in the tight control group, which suggests a target range of 144-180 is best for optimal outcomes (NICE Sugar Study Investigators, 2009).
In 2007, patient’s with diabetes accounted for 40.7 million inpatient days. This is representative of 22% of the 186 million hospital days accrued by the general population (Kirk & Oldham, 2010). The proportion of US surgical patients who have diabetes ranges 15-20%. The percentage may be greater for patient’s undergoing cardiothoracic surgery. A prospective study found that patient’s with hyperglycemia (at least 1 serum glucose level greater than 200 mg/dl) at day 1 post-surgery, had a nosocomial infection rate 2.7 times greater than those without hyperglycemia. Hyperglycemia at day 1 post-surgery was associated with a 5-fold increased risk for infection (Kirk & Oldham, 2010).
Insulin is the treatment of choice for hyperglycemia in hospitalized patients because insulin doses can be titrated and evaluated in an expeditious manner. A physiologic insulin regimen is suggested for optimal outcomes. Basal insulin is the insulin normally released continuously by the pancreas, even when fasting. This serves to suppress glucose and ketone production (Wesorick, O’Malley, Rushakoff, Larsen & Magee, 2008). The recommended starting subcutaneous insulin protocol for patients receiving meals is a basal-bolus approach using 0.4 -0.5 U/kg basal insulin (glargine once daily or neutral protamine Hagedorn [NPH] twice daily) and 0.1 U/kg rapid analog at each meal (lispro, aspart or glulisine) . The dose of basal is lowered by 0.2 U/kg for medical conditions with a high sensitivity to insulin or that have an added risk for hypoglycemia (renal or hepatic impairment, thin or normal weight, elderly, frail, hypothyroidism, adrenal insufficiency, etc.). For states of high insulin resistance, such as marked obesity, metabolic syndrome, open wounds and infection, an extra 0.2 U/kg may be given. Pre-mixed insulin is not suggested for inpatient use because there is no allowance for each component to be separately titrated in response to each patient’s insulin needs (Moghissi, 2010). If the last HgbA1C was performed more than 30 days before admission or is not available, one should be obtained upon hospital admission to help guide both inpatient and discharge therapy (O’Malley, Emanuele, Halasyamani & Amin, 2008).
A correctional insulin dose provides an insulin adjustment based on the pre-prandial glucose value. This correctional dose resembles a sliding scale, but is only a small fine-tuning insulin adjustment (Nau, Lorenzetti, Cuczzella, Devine & Kline, 2010). Correctional scale can vary and categorized as low, medium and high intensity. Low intensity correction is typically 1 unit to drop 50 points and is selected for patients who are either/or lean, elderly, type 1 diabetics or have kidney disease. Moderate intensity correction is typically 1 unit to drop 25 points and used for most patients – BMI 25-35. High intensity correction is typically 1 unit to drop 15 points and used along with steroids, if infections along with sepsis are present, extreme insulin resistance and BMI greater than 35 (Nau, Lorenzetti, Cucuzzella, Devine & Kline, 2010).
Nutritional insulin is an additional component and covers for the blood sugar excursions that occur after the ingestion of food. Once food has been ingested, there is a surge of blood glucose, this surge is accompanied by a rapid secretion of additional insulin for glucose utilization (Wesorick, O’Malley, Rushakoff, Larsen & Magee, 2008).
If correctional insulin is required consistently or in high doses, the basal insulin and/or nutritional insulin should be modified. A proportion of the total number of units of correctional insulin given in the preceding 24 ours can be distribured into basal and nutritional insulin doses for the next day (Wesorick, O’Malley, Rushakoff, Larsen & Magee, 2008).
Type 1 diabetics require special considerations and require continuous, exogenous basal insulin even when fasting. Failure to provide basal insulin can lead to ketoacidosis. When receiving nutrition, type 1 diabetics also require nutritional and correctional insulin. Typically type 1 diabetics are insulin sensitive and require less insulin than type 2 diabetics to achieve blood sugar control (Wesorick, O’Malley, Rushakoff, Larsen & Magee, 2008).
Many patients are “nothing by mouth” (NPO) for most procedures. NPO can mean missing a single meal during the day and, for others, it can mean missing several meals. Many of these patients require insulin to control their blood sugars. The strategy for insulin management with these patients should mimic physiologic insulin secretion, in other words, a basal plus a calorie-stimulated bolus of insulin. Even if the patient is NPO, basal insulin replacement should be continued. If the basal insulin is removed, diabetes control will be more difficult from the start. A suggested strategy is to use one half to two-thirds of the patient’s usual basal insulin dose the evening before and the morning of surgery – with the option to give a full dose (Wesorick, O’Malley, Rushakoff, Larsen & Magee, 2008). Preoperatively, blood sugar targets should be less than 200 – higher levels can cause neutrophil dysfunction thus compromising bacterial killing (Smiley & Umpierrez, 2010). Sulfonylureas and thiazolidinediones can typically be stopped the morning of surgery. Metformin is typically stopped 48 hours before a surgical procedure and not administered during hospitalization.
Enteral feedings can also pose a problem with blood sugar control. During enteral feeding, a compound called glucagon-like-peptide-1 stimulates the pancreas to produce more insulin. When the tube feeding is given at a continuous rate over 24 hours, frequent administration of intermediate and short acting insulin simulates continuous insulin administration is recommended. To cover for nutritional needs of a patient receiving continuous enteral tube feedings, an initial plan for small doses of NPH every 6-8 hours can be safer than a plan for larger doses of NPH given every 12 hours (Cook, Burkitt, McDonald & Sublett, 2009). If the tube feeding is held, to prevent hypoglycemia and ensure safety, standing orders to substitute IV 10% dextrose in water (D10W) at the same rate as the prior tube feeds should be in place (O’Malley, Emanuele, Halasyamani & Amin, 2008).
Wounds should be evaluated for an infection when blood sugars are reasonably well controlled during hospitalization and blood sugars experience an unexpected elevation. One study that examined post operative diabetic patients found that in patients with at least one glucose measurement greater than 220 on the first postoperative day, the infection rate was 2.7 times that observed in diabetic patients with all glucose measurements below 220 – and the risk for a serious infection was 5.8 times greater. Glucose levels are a sensitive marker for counter-regulatory hormones. These counter-regulatory hormones can become activated before a patient becomes febrile. The primary mechanism responsible for the increased risk of infection with hyperglycemia is phagocyte dysfunction. Hyperglycemia also increases inflammatory cytokines, oxidative stress and decreases the immune, cardiovascular and nervous system response (Moghissi, 2010).
Glucocorticoids increase the need of insulin requirements in many patients. The effect of glucocorticoids on blood sugars can vary a great deal from patient to patient. Steroids create hyperglycemia by stimulating hepatic gluconeogensis, peripheral insulin resistance and diminish insulin secretion (Donner & Flammer, 2008). Hyperglycemia induced from a steroid dose will most likely peak 8-12 hours after it is given. NPH insulin is ideal in these cases because the peak and onset times closely mimic the peak and onset of most glucocorticoids (Maynard, Wesorick, O’Malley & Inzucchi, 2012).
Total parenteral nutrition (TPN) also creates hyperglycemic excursions. TPN may double a patient’s insulin requirement. Hyperglycemia evolves from the high carbohydrate content in the TPN and intravenous nutrition bypasses intestinal regulators of glucose metabolism. One commonly used strategy is to add regular insulin to the TPN bag – typically at 1 unit/10g of infused carbohydrate. Insulin dosing in the TPN bag is titrated according to the amount of supplemental insulin used – typically 80% of the supplemental insulin requirement can be added to the TPN bag for the following day (Wesorick, O’Malley, Rushakoff, Larsen & Magee, 2008). .
Achieving good blood sugar control for our inpatient diabetes population can be complicated, time consuming and labor intensive. At the same time, achieving good blood sugar control for this population has the opportunity to yield a remarkable improvement in patient outcomes.
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