Treating Hyperglycemia and Diabetes With Insulin Therapy

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Treating Hyperglycemia and Diabetes With Insulin Therapy: Transition From Inpatient to Outpatient Care CME
Posted 09/17/2008
Frank Lavernia, MD
From The Medscape Journal of Medicine

Abstract and Introduction

Abstract

Context: Intensive insulin therapy is recommended to control glucose elevations in the critically ill and has been shown to significantly improve outcomes among hospital inpatients with acute hyperglycemia or newly diagnosed diabetes. Once discharged, the hyperglycemic patient may require ongoing outpatient care, most often under the attention of a primary care physician.
Evidence acquisition: The purpose of this review is to provide a background of in-hospital hyperglycemia management and discharge planning in preparation for continued outpatient care. Primary data sources were identified through a PubMed search (1990-2007) using keywords, such as diabetes, hyperglycemia, in-hospital, discharge, and insulin.

Evidence synthesis: Hyperglycemia protocols with strict glycemic goals have been shown to improve morbidity and mortality among critically ill inpatients. Discharge planning should prepare patients for self-care and give them the survival skills necessary to maintain glycemic control. In preparation for discharge, patients are usually transitioned from insulin infusions to subcutaneous insulin administered through an appropriate basal-prandial regimen.
Conclusion: A thorough understanding of hyperglycemia history and treatment will allow the primary care physician to deliver optimal diabetes care and thereby improve both short-term and long-term outcomes for those patients with critical illnesses and hyperglycemia or diabetes.

Introduction

Hyperglycemia, when left untreated, can have a negative impact on the patient's prognosis and outcome during the hospital stay and after discharge.[1-5] The prevalence of hyperglycemia in hospitalized patients is high, and may be associated with multiple factors: First, about 20.8 million Americans have diabetes, 6.2 million of whom (around one third) have not been diagnosed.[1,6] Furthermore, diabetes itself may contribute to hospitalization because it can lead to cardiovascular disease, renal damage, stroke, and/or other complications.[7-9] Finally, hyperglycemia may be induced during periods of acute metabolic stress or traumatic injury, develop as a result of surgery, or arise as an adverse effect of treatment with certain medications.[2, 9-11] Several investigators have reported newly occurring hyperglycemia in association with acute hospital admissions, and others have shown the progression from normal glucose homeostasis to hyperglycemia during critical illnesses.[12,13] Cely and colleagues[13] found that among medical inpatients, even those with normal baseline glucose levels had hyperglycemia for at least a portion of time while in the intensive care unit (ICU), with duration of hyperglycemia increasing by 19% for each 1.0% increase in glycated hemoglobin A1C (A1C) (Figure 1).[13] For many individuals, therefore, plasma glucose is an important consideration during in-hospital medical care.

Thus, identifying hyperglycemia in new critically ill inpatients is a medical priority necessary to ensure optimal care and improved outcomes. Table 1 lists parameters for normoglycemia and glycemic targets for most patients.[7,14,15] The American Diabetes Association (ADA) also specifies that in critically ill patients, blood glucose values should be kept as close to 110 mg/dL as possible and generally under 140 mg/dL.[7] Stress hyperglycemia and diabetes have been associated with a significantly higher mortality rate, increased length of hospital stay, poor cardiovascular outcomes, and greater need for ICU admission compared with normoglycemia.[1,3,4] In fact, Umpierrez and colleagues[1] reported an in-hospital mortality rate 3 times higher in ICU patients with new hyperglycemia (no prior history of diabetes and admission or in-hospital fasting glucose level > 126 mg/dL or random blood glucose level > 200 mg/dL on &#8805; 2 determinations) than in those with normoglycemia (31% vs 10%, P < .01), and 3 times higher than in patients with known diabetes (31% vs 11%, P < .01). Furthermore, this increase in mortality was also evident in non-ICU patients and in both groups combined.

Even small elevations in glucose can substantially increase morbidity and mortality. Krinsley[5] noted that mortality among 1826 critically ill ICU patients increased in parallel with advancing glucose levels but was elevated even at the relatively modest mean glucose levels of 100-119 mg/dL. As a result, it would appear that treatment to reduce glucose might improve the prognosis for all critically ill hospitalized inpatients.

Several investigators have established that controlling glucose with intensive insulin therapy (IIT) during hospitalization reduces morbidity and mortality among critically ill individuals. Working primarily with patients undergoing cardiac surgery, researchers have found that perioperative intensive insulin infusion (to maintain blood glucose at predefined levels ranging variably between 80 mg/dL and 150 mg/dL in different studies) significantly improves both short-term (in-hospital) morbidity and mortality[16-18] and long-term (postdischarge) patient outcomes.[19] Furthermore, many of these patients with hyperglycemia and diabetes will require ongoing monitoring and continued glucose-lowering therapy after discharge, once they have returned to the care of a primary care physician (PCP). Thus, PCPs increasingly need to understand the metabolic changes associated with stress hyperglycemia, to become familiar with the in-hospital regimens used to reduce elevated blood glucose levels, and to learn how to help with the transition from inpatient insulin therapy to long-term glycemic care. This article provides background establishing the correlation between hyperglycemia and morbidity and mortality and reviews how hyperglycemia is managed in the hospital and how this affects the responsibility of PCPs as long-term care providers.

Medscape J Med. 2008; 10(9):216. ©2008 Medscape