Isosorbide dinitrate-hydralazine improves outcomes in African Americans with heart failure

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Interpreting the African American Heart Failure Trial (A-HeFT)
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Interpreting the African American Heart Failure Trial (A-HeFT)
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If you have celiac disease

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Update on hormonal contraception

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An elderly woman with severe anemia

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Current and Emerging Therapeutic Modalities for Hyperhidrosis, Part 1: Conservative and Noninvasive Treatments

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EXCLUSIVELY ON THE WEBCo-surgery: Both surgeons bill, with modifier ... Delay doesn't change coding for surgical tx of incomplete abortion

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Co-surgery: Both surgeons bill, with modifier ... Delay doesn't change coding for surgical tx of incomplete abortion

Co-surgery: Both surgeons bill, with modifier

Q. I was called in to provide intraoperative consultation for a neighboring general surgeon. He had performed an exploratory laparotomy, and the only finding was a pedunculated fibroid. I performed a myomectomy, assisted by the general surgeon. He had begun the procedure with his physician assistant and finished assisted by the PA after I finished my part. What is the best way to code for this situation?

A. Under CPT guidelines that were clarified in the American Medical Association’s May 1997 “CPT Assistant,” this is a co-surgery case because (1) establishing the operative site and exploration are integral to the procedure and (2) you both performed a distinct part of the procedure. You and the general surgeon would use the same surgical code with a modifier -62 [Two surgeons]. Your code choice for this procedure would be 58140 [Myomectomy, excision of fibroid tumor(s) of uterus, 1 to 4 intramural myoma(s) with total weight of 250 grams or less and/or removal of surface myomas; abdominal approach].

The general surgeon should also bill for the surgical assistant services of the PA by adding a modifier AS [Physician assistant, nurse practitioner, or clinical nurse specialist services for assistant at surgery] to this same surgical code. Some payers might deny an assistant in a co-surgery case, but the documentation in this situation would support the need because the PA assisted only when you were not present.

Delay doesn’t change coding for surgical tx of incomplete abortion

Q. I recently performed a suction D&C for an incomplete voluntary abortion done 2 months ago that was hemorrhaging and had retained products of conception. Our billing department coded this as 59840, but the payer rejected the claim, stating that they already paid the hospital for 59812, which I thought was reported only for a spontaneous abortion. Should we refile?

A. Yes. At this point, you are removing retained products of conception no matter what the patient intended 2 months ago. This means that you are performing a surgical treatment of an incomplete abortion, coded 59812. Code 59840 implies that you are the one inducing the abortion at this surgical session—not the case.

The diagnosis for bleeding after an abortion performed at a previous surgery is 639.1.

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Co-surgery: Both surgeons bill, with modifier

Q. I was called in to provide intraoperative consultation for a neighboring general surgeon. He had performed an exploratory laparotomy, and the only finding was a pedunculated fibroid. I performed a myomectomy, assisted by the general surgeon. He had begun the procedure with his physician assistant and finished assisted by the PA after I finished my part. What is the best way to code for this situation?

A. Under CPT guidelines that were clarified in the American Medical Association’s May 1997 “CPT Assistant,” this is a co-surgery case because (1) establishing the operative site and exploration are integral to the procedure and (2) you both performed a distinct part of the procedure. You and the general surgeon would use the same surgical code with a modifier -62 [Two surgeons]. Your code choice for this procedure would be 58140 [Myomectomy, excision of fibroid tumor(s) of uterus, 1 to 4 intramural myoma(s) with total weight of 250 grams or less and/or removal of surface myomas; abdominal approach].

The general surgeon should also bill for the surgical assistant services of the PA by adding a modifier AS [Physician assistant, nurse practitioner, or clinical nurse specialist services for assistant at surgery] to this same surgical code. Some payers might deny an assistant in a co-surgery case, but the documentation in this situation would support the need because the PA assisted only when you were not present.

Delay doesn’t change coding for surgical tx of incomplete abortion

Q. I recently performed a suction D&C for an incomplete voluntary abortion done 2 months ago that was hemorrhaging and had retained products of conception. Our billing department coded this as 59840, but the payer rejected the claim, stating that they already paid the hospital for 59812, which I thought was reported only for a spontaneous abortion. Should we refile?

A. Yes. At this point, you are removing retained products of conception no matter what the patient intended 2 months ago. This means that you are performing a surgical treatment of an incomplete abortion, coded 59812. Code 59840 implies that you are the one inducing the abortion at this surgical session—not the case.

The diagnosis for bleeding after an abortion performed at a previous surgery is 639.1.

Co-surgery: Both surgeons bill, with modifier

Q. I was called in to provide intraoperative consultation for a neighboring general surgeon. He had performed an exploratory laparotomy, and the only finding was a pedunculated fibroid. I performed a myomectomy, assisted by the general surgeon. He had begun the procedure with his physician assistant and finished assisted by the PA after I finished my part. What is the best way to code for this situation?

A. Under CPT guidelines that were clarified in the American Medical Association’s May 1997 “CPT Assistant,” this is a co-surgery case because (1) establishing the operative site and exploration are integral to the procedure and (2) you both performed a distinct part of the procedure. You and the general surgeon would use the same surgical code with a modifier -62 [Two surgeons]. Your code choice for this procedure would be 58140 [Myomectomy, excision of fibroid tumor(s) of uterus, 1 to 4 intramural myoma(s) with total weight of 250 grams or less and/or removal of surface myomas; abdominal approach].

The general surgeon should also bill for the surgical assistant services of the PA by adding a modifier AS [Physician assistant, nurse practitioner, or clinical nurse specialist services for assistant at surgery] to this same surgical code. Some payers might deny an assistant in a co-surgery case, but the documentation in this situation would support the need because the PA assisted only when you were not present.

Delay doesn’t change coding for surgical tx of incomplete abortion

Q. I recently performed a suction D&C for an incomplete voluntary abortion done 2 months ago that was hemorrhaging and had retained products of conception. Our billing department coded this as 59840, but the payer rejected the claim, stating that they already paid the hospital for 59812, which I thought was reported only for a spontaneous abortion. Should we refile?

A. Yes. At this point, you are removing retained products of conception no matter what the patient intended 2 months ago. This means that you are performing a surgical treatment of an incomplete abortion, coded 59812. Code 59840 implies that you are the one inducing the abortion at this surgical session—not the case.

The diagnosis for bleeding after an abortion performed at a previous surgery is 639.1.

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Multisite injection might not be reimbursed as multiple procedures ... Split preop visit from surgery? Maybe

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Multisite injection might not be reimbursed as multiple procedures

Q. I have been injecting lidocaine in a grid pattern into the vulvar area of some of my patients to treat vestibulitis. Is there a specific CPT code for this procedure?

A. Although CPT includes codes for injection into nerves [eg, 64430, Injection, anesthetic agent; pudendal nerve], lesions [eg, 11900, Injection, intralesional; up to and including seven lesions], and trigger-point muscles [eg, 20552, Injection(s); single or multiple trigger point(s), one or two muscle(s)], it appears that the local anesthetic you are injecting is being placed subcutaneously. This means that code 90772 [Therapeutic, prophylactic or diagnostic injection (specify substance or drug); subcutaneous or intramuscular] is the correct code.

What may present a problem, however, is that you are administering lidocaine in several areas of the vulva. Many payers have a unit limitation for the number of injections you can bill at one time; if you use the same syringe and needle for injection at multiple sites, the payer may decide to reimburse for only a single injection.

Some practices have been successful in getting fair reimbursement by billing code 58999 [Unlisted procedure, female genital system (nonobstetrical)] for this treatment.

If you will be billing the injection procedure instead, note that the “J” code for lidocaine was deleted in 2006. To bill for lidocaine, report J3490 [Unclassified drugs]. Lidocaine would be included as a supply with code 58999 and therefore not separately billable.

Split preop visit from surgery? Maybe

Q. When a procedure (such as hysteroscopy) has no global days and the decision to perform the surgery was made at a previous visit (perhaps days or weeks before the procedure), can we bill a preoperative visit that is made the week of the surgery? This visit involves talking to the patient to answer any additional questions, taking a history and performing a physical exam, providing preadmission and preoperative instructions, and having her sign the informed consent form.

A. There isn’t any black-and-white answer; the payer determines the coverage. Many payers consider the service that you are describing integral to performing any surgery and therefore included in the billing for the procedure—especially if the visit occurred within 48 hours before planned surgery.

Some payers will reimburse for this visit, however, and you owe it to them to indicate the nature of the visit. This means that you should not provide a diagnosis code for the visit that is the actual reason for doing the surgery; instead, code V72.83 [other specified preop exam] or V72.84 [unspecified preop exam]. This allows the payer to apply its policy on this matter. A payer that includes the preop exam will deny the claim; one that doesn’t, will reimburse you.

There’s more Adviser for you on the Web

One surgery, two surgeons: How do both code to be reimbursed? Find the answer and read more “Reimbursement Adviser” on the Web at www.obgmanagement.com

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Multisite injection might not be reimbursed as multiple procedures

Q. I have been injecting lidocaine in a grid pattern into the vulvar area of some of my patients to treat vestibulitis. Is there a specific CPT code for this procedure?

A. Although CPT includes codes for injection into nerves [eg, 64430, Injection, anesthetic agent; pudendal nerve], lesions [eg, 11900, Injection, intralesional; up to and including seven lesions], and trigger-point muscles [eg, 20552, Injection(s); single or multiple trigger point(s), one or two muscle(s)], it appears that the local anesthetic you are injecting is being placed subcutaneously. This means that code 90772 [Therapeutic, prophylactic or diagnostic injection (specify substance or drug); subcutaneous or intramuscular] is the correct code.

What may present a problem, however, is that you are administering lidocaine in several areas of the vulva. Many payers have a unit limitation for the number of injections you can bill at one time; if you use the same syringe and needle for injection at multiple sites, the payer may decide to reimburse for only a single injection.

Some practices have been successful in getting fair reimbursement by billing code 58999 [Unlisted procedure, female genital system (nonobstetrical)] for this treatment.

If you will be billing the injection procedure instead, note that the “J” code for lidocaine was deleted in 2006. To bill for lidocaine, report J3490 [Unclassified drugs]. Lidocaine would be included as a supply with code 58999 and therefore not separately billable.

Split preop visit from surgery? Maybe

Q. When a procedure (such as hysteroscopy) has no global days and the decision to perform the surgery was made at a previous visit (perhaps days or weeks before the procedure), can we bill a preoperative visit that is made the week of the surgery? This visit involves talking to the patient to answer any additional questions, taking a history and performing a physical exam, providing preadmission and preoperative instructions, and having her sign the informed consent form.

A. There isn’t any black-and-white answer; the payer determines the coverage. Many payers consider the service that you are describing integral to performing any surgery and therefore included in the billing for the procedure—especially if the visit occurred within 48 hours before planned surgery.

Some payers will reimburse for this visit, however, and you owe it to them to indicate the nature of the visit. This means that you should not provide a diagnosis code for the visit that is the actual reason for doing the surgery; instead, code V72.83 [other specified preop exam] or V72.84 [unspecified preop exam]. This allows the payer to apply its policy on this matter. A payer that includes the preop exam will deny the claim; one that doesn’t, will reimburse you.

There’s more Adviser for you on the Web

One surgery, two surgeons: How do both code to be reimbursed? Find the answer and read more “Reimbursement Adviser” on the Web at www.obgmanagement.com

Multisite injection might not be reimbursed as multiple procedures

Q. I have been injecting lidocaine in a grid pattern into the vulvar area of some of my patients to treat vestibulitis. Is there a specific CPT code for this procedure?

A. Although CPT includes codes for injection into nerves [eg, 64430, Injection, anesthetic agent; pudendal nerve], lesions [eg, 11900, Injection, intralesional; up to and including seven lesions], and trigger-point muscles [eg, 20552, Injection(s); single or multiple trigger point(s), one or two muscle(s)], it appears that the local anesthetic you are injecting is being placed subcutaneously. This means that code 90772 [Therapeutic, prophylactic or diagnostic injection (specify substance or drug); subcutaneous or intramuscular] is the correct code.

What may present a problem, however, is that you are administering lidocaine in several areas of the vulva. Many payers have a unit limitation for the number of injections you can bill at one time; if you use the same syringe and needle for injection at multiple sites, the payer may decide to reimburse for only a single injection.

Some practices have been successful in getting fair reimbursement by billing code 58999 [Unlisted procedure, female genital system (nonobstetrical)] for this treatment.

If you will be billing the injection procedure instead, note that the “J” code for lidocaine was deleted in 2006. To bill for lidocaine, report J3490 [Unclassified drugs]. Lidocaine would be included as a supply with code 58999 and therefore not separately billable.

Split preop visit from surgery? Maybe

Q. When a procedure (such as hysteroscopy) has no global days and the decision to perform the surgery was made at a previous visit (perhaps days or weeks before the procedure), can we bill a preoperative visit that is made the week of the surgery? This visit involves talking to the patient to answer any additional questions, taking a history and performing a physical exam, providing preadmission and preoperative instructions, and having her sign the informed consent form.

A. There isn’t any black-and-white answer; the payer determines the coverage. Many payers consider the service that you are describing integral to performing any surgery and therefore included in the billing for the procedure—especially if the visit occurred within 48 hours before planned surgery.

Some payers will reimburse for this visit, however, and you owe it to them to indicate the nature of the visit. This means that you should not provide a diagnosis code for the visit that is the actual reason for doing the surgery; instead, code V72.83 [other specified preop exam] or V72.84 [unspecified preop exam]. This allows the payer to apply its policy on this matter. A payer that includes the preop exam will deny the claim; one that doesn’t, will reimburse you.

There’s more Adviser for you on the Web

One surgery, two surgeons: How do both code to be reimbursed? Find the answer and read more “Reimbursement Adviser” on the Web at www.obgmanagement.com

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What are the disadvantages of sliding‐scale insulin?

Tight glycemic control in the hospitalized patient is not a simple task. Hospitalized patients are characterized by high levels of counterregulatory hormones (catecholamines, cortisol, and growth hormone) and cytokines that vary greatly in the context of sepsis, burns, hypoxia, cardiovascular disease, pain, surgery, and trauma. In addition, inpatients have unpredictable eating times and little to no physical activity. Each of the major classes of oral glycemic agents has significant limitations for inpatient use and provides little flexibility or opportunity for titration in a setting where acute changes demand these qualities. As a result, sliding‐scale insulin (SSI) regimens are often used to treat hyperglycemia in patients with or without diabetes in these clinical situations.

SSI usually consists of rapid‐acting or regular insulin ordered in a specified number of units for a given degree of hyperglycemia without regard to the timing of food, any preexisting insulin administration, or even individualization of a patient's sensitivity to insulin. This is not a physiologic approach to insulin management and not an ideal strategy for managing hyperglycemia. Because many SSI regimens do not initiate therapy until the blood glucose level is more than 200 mg/dL, SSI uses hyperglycemia as a threshold. This allows hyperglycemia to persist for long periods without intervention. In turn, SSI is reactive instead of proactive. With SSI, the current dose of insulin is based on the inadequacy of the previous dose, creating a chase‐your‐tail phenomenon. In addition, once the SSI regimen begins, glycemic control is rarely assessed by a physician until blood glucose is dangerously low or high (60 or >400 mg/dL). Finally, SSI provides no basal insulin. Hospitalized patients with stress‐induced hyperglycemia require not only postprandial insulin but also basal insulin to control blood glucose between meals and at night.

Evidence supporting SSI as a primary method of blood glucose control in diabetic patients is lacking. A search of MEDLINE for the period from 1966 to 2003 with the terms sliding scale insulin, sliding scale, and sliding combined with insulin yielded a total of 52 publications, none of which showed a benefit of sliding‐scale insulin in improving glycemic control or clinical outcomes. Retrospective and nonrandomized studies confirmed that SSI is associated with more hyper‐ and hypoglycemia with longer hospital stays.13 Queale et al. published the largest prospective cohort study (n = 171) of diabetic patients on SSI.4 More than 40% had at least one episode of hyperglycemia (>300 mg/dL), and 25% had more than one episode. Use of SSI alone increased the likelihood of hyperglycemia 3‐fold. Hypoglycemia occurred in 23%. Despite this poor performance in controlling blood glucose, the SSI remained unadjusted throughout the hospital stay for more than 80% of patients. In total, the clinical studies and clinical reviews on SSI confirmed that it is an inappropriate approach to blood glucose control in diabetic patients. Yet, SSI use in the inpatient setting continues to be a routine passed down from attending physicians to residents and medical students. In one recent study, 61% of diabetic patients admitted to the hospital for reasons other than metabolic control were on SSI.5 This sliding‐scale culture tolerates hyperglycemia and relieves the burden on the medical team to closely manage the glucose. Clinicians rely on the SSI to manage hyperglycemia rather than make frequent insulin adjustments.

Insulin, given either intravenously as a continuous infusion or subcutaneously, is the most effective agent for achieving glycemic control in hospitalized patients. Intravenous insulin infusions have been used for many years and have a proven track record for efficacy and safety. It does require frequent bedside blood glucose monitoring, which may limit its use on regular medical floors. The ideal frequency for monitoring has not been studied, but it is generally recommended that blood glucose be tested every hour until a stable infusion rate is reached. Unlike SSI, effective subcutaneous insulin therapy should define the dose components physiologically in the form of basal, nutritional or prandial, and correction doses (Fig. 1). Basal insulin is a patient's baseline level of insulin available throughout the day. Basal insulin gives the patient enough insulin to suppress hepatic glucose output, and it keeps the body from becoming hyperglycemic and ketoacidotic when not eating. Nutritional insulin is defined as the insulin needed to cover any intravenous glucose the patient is receiving, intravenous or enteral alimentation, and calories consumed in meals. If the patient is eating and is not receiving any other sources of calories, nutritional insulin would be the same as prandial insulin. In addition to basal and nutritional insulin requirements, patients often require supplemental or correction doses of insulin to treat unexpected hyperglycemia. Therefore, subcutaneous insulin can be given as a scheduled or programmed dose (basal + nutritional) and then a rapid‐acting supplemental (correction) dose to cover any hyperglycemia above target. The supplemental dose should not be confused with SSI, which does not provide any programmed basal and nutritional insulin. To provide the right amounts of basal and prandial insulin, you need to choose from the available therapies by examining their properties (Table 1). The ideal basal insulin should be long acting without identifiable peaks in concentration. For patients who are not eating, nutritional doses can be programmed with intermediate‐acting insulin. When giving insulin to patients before meals, rapid‐acting insulin analogs are best suited for the hospitalized patient because of their short onset of action. Regular insulin is also short acting, but it takes 30 minutes to take effect; thus, the dose needs to be timed at least a half hour prior to the meal. In addition, regular insulin can last for 6‐8 hours if large doses are used, which is not an ideal quality to have if trying to control postprandial glucose. The best way to mimic normal physiology is to use a combination of several types of insulin. A common strategy is to give a single daily injection of basal insulin (glargine/detimir) and then use rapid‐acting insulin analogs (lispro/aspart/glulisine) to cover prandial and correction doses.

Figure 1
Physiologic insulin requirements of healthy and sick patients.
Insulin Types
Time to Action Peak Duration
Lispro/aspart/glulisine 5‐15 minutes 1‐2 hours 3‐6 hours
Human NPH 1‐2 hours 4‐8 hours 10‐20 hours
Regular/human 30‐60 minutes 2‐4 hours 6‐10 hours
Glargine/detimir 1‐2 hours Flat 24 hours

The initial doses of scheduled subcutaneous insulin are based on previously established dose requirements, previous experience of the same patient during similar circumstances, requirements during a stable continuous insulin infusion, and/or knowledge of how stable medical condition and nutritional intake are. For patients whose insulin requirements are unknown and whose nutritional intake will be adequate, a reasonable assumption based on body weight is 0.5‐0.7 units/kg per 24 hours. Type 2 diabetics may need more, however; regardless, the patient's regimen should be started low and worked up to the dose to meet the demonstrated need. For type 1 diabetics with limited nutritional intake, the amount of scheduled insulin calculated by body weight should be reduced by 50%. For type 2 diabetics with limited nutritional intake, endogenous insulin may be adequate for basal requirements, and until results of monitoring indicate a further need for scheduled insulin, only correction doses should be used initially.

Many patients will need to transition from intravenous to subcutaneous insulin therapy when transferred from the critical care unit to the regular nursing floor. To maintain effective blood levels of insulin, it is necessary to administer short‐ or rapid‐acting insulin subcutaneously 1‐2 hours before or intermediate‐ or long‐acting insulin 2‐3 hours before stopping the insulin infusion. Subcutaneous insulin with an appropriate duration of action may be administered as a single dose or repeatedly to maintain basal effect until the time of day when insulin or analog, whichever preferred for basal effect, normally would be provided. For example, patients who typically receive glargine at night but have their insulin infusion stopped at lunchtime could receive a one‐time dose of NPH before interruption of the insulin infusion.

Hypoglycemia is a concern in hospitalized patients with diabetes, and it has been a major barrier to aggressive treatment of hyperglycemia in the hospital. Yet hypoglycemia can be predicted and prevented. Factors that increase the risk of hypoglycemia in the hospital include inadequate glucose monitoring; lack of clear communication or coordination between dietary, transportation, and nursing staff; and illegible orders.6 Clear algorithms for insulin orders and clear hypoglycemia protocols will reduce the likelihood of severe hypoglycemia occurring.

Although most positive outcomes associated with the new glycemic targets are derived from the critical care setting, there is a rationale supporting their benefit for other patients. The current glycemic targets for hospitalized patients warrant an approach that stresses the use of insulin in a way that matches normal physiology. The traditional SSI regimen is ineffective, and using it to manage glucose in the inpatient setting can no longer be justified.

References
  1. Gearhart JG,Duncan JL,Replogle WH,Forbes RC,Walley EJ.Efficacy of sliding‐scale insulin therapy: a comparison with prospective regimens.Fam Pract Res J.1994;14:313321.
  2. Smith WD,Winterstein AG,Johns T,Rosenberg E,Sauer B.Causes of hyperglycemia and hypoglycemia in adult inpatients.Am J Health Syst Pharm.2005;62:714719.
  3. Browning LA,Dumo P.Sliding‐scale insulin: an antiquated approach to glycemic control in hospitalized patients.Am J Health Syst Pharm.2004;61:16111614.
  4. Queale WS,Seidler AJ,Brancati FL.Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus.Arch Intern Med.1997;157:545552.
  5. Moghissi E.Hospital management of diabetes: beyond the sliding scale.Cleve Clin J Med.2004;71:801808.
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Tight glycemic control in the hospitalized patient is not a simple task. Hospitalized patients are characterized by high levels of counterregulatory hormones (catecholamines, cortisol, and growth hormone) and cytokines that vary greatly in the context of sepsis, burns, hypoxia, cardiovascular disease, pain, surgery, and trauma. In addition, inpatients have unpredictable eating times and little to no physical activity. Each of the major classes of oral glycemic agents has significant limitations for inpatient use and provides little flexibility or opportunity for titration in a setting where acute changes demand these qualities. As a result, sliding‐scale insulin (SSI) regimens are often used to treat hyperglycemia in patients with or without diabetes in these clinical situations.

SSI usually consists of rapid‐acting or regular insulin ordered in a specified number of units for a given degree of hyperglycemia without regard to the timing of food, any preexisting insulin administration, or even individualization of a patient's sensitivity to insulin. This is not a physiologic approach to insulin management and not an ideal strategy for managing hyperglycemia. Because many SSI regimens do not initiate therapy until the blood glucose level is more than 200 mg/dL, SSI uses hyperglycemia as a threshold. This allows hyperglycemia to persist for long periods without intervention. In turn, SSI is reactive instead of proactive. With SSI, the current dose of insulin is based on the inadequacy of the previous dose, creating a chase‐your‐tail phenomenon. In addition, once the SSI regimen begins, glycemic control is rarely assessed by a physician until blood glucose is dangerously low or high (60 or >400 mg/dL). Finally, SSI provides no basal insulin. Hospitalized patients with stress‐induced hyperglycemia require not only postprandial insulin but also basal insulin to control blood glucose between meals and at night.

Evidence supporting SSI as a primary method of blood glucose control in diabetic patients is lacking. A search of MEDLINE for the period from 1966 to 2003 with the terms sliding scale insulin, sliding scale, and sliding combined with insulin yielded a total of 52 publications, none of which showed a benefit of sliding‐scale insulin in improving glycemic control or clinical outcomes. Retrospective and nonrandomized studies confirmed that SSI is associated with more hyper‐ and hypoglycemia with longer hospital stays.13 Queale et al. published the largest prospective cohort study (n = 171) of diabetic patients on SSI.4 More than 40% had at least one episode of hyperglycemia (>300 mg/dL), and 25% had more than one episode. Use of SSI alone increased the likelihood of hyperglycemia 3‐fold. Hypoglycemia occurred in 23%. Despite this poor performance in controlling blood glucose, the SSI remained unadjusted throughout the hospital stay for more than 80% of patients. In total, the clinical studies and clinical reviews on SSI confirmed that it is an inappropriate approach to blood glucose control in diabetic patients. Yet, SSI use in the inpatient setting continues to be a routine passed down from attending physicians to residents and medical students. In one recent study, 61% of diabetic patients admitted to the hospital for reasons other than metabolic control were on SSI.5 This sliding‐scale culture tolerates hyperglycemia and relieves the burden on the medical team to closely manage the glucose. Clinicians rely on the SSI to manage hyperglycemia rather than make frequent insulin adjustments.

Insulin, given either intravenously as a continuous infusion or subcutaneously, is the most effective agent for achieving glycemic control in hospitalized patients. Intravenous insulin infusions have been used for many years and have a proven track record for efficacy and safety. It does require frequent bedside blood glucose monitoring, which may limit its use on regular medical floors. The ideal frequency for monitoring has not been studied, but it is generally recommended that blood glucose be tested every hour until a stable infusion rate is reached. Unlike SSI, effective subcutaneous insulin therapy should define the dose components physiologically in the form of basal, nutritional or prandial, and correction doses (Fig. 1). Basal insulin is a patient's baseline level of insulin available throughout the day. Basal insulin gives the patient enough insulin to suppress hepatic glucose output, and it keeps the body from becoming hyperglycemic and ketoacidotic when not eating. Nutritional insulin is defined as the insulin needed to cover any intravenous glucose the patient is receiving, intravenous or enteral alimentation, and calories consumed in meals. If the patient is eating and is not receiving any other sources of calories, nutritional insulin would be the same as prandial insulin. In addition to basal and nutritional insulin requirements, patients often require supplemental or correction doses of insulin to treat unexpected hyperglycemia. Therefore, subcutaneous insulin can be given as a scheduled or programmed dose (basal + nutritional) and then a rapid‐acting supplemental (correction) dose to cover any hyperglycemia above target. The supplemental dose should not be confused with SSI, which does not provide any programmed basal and nutritional insulin. To provide the right amounts of basal and prandial insulin, you need to choose from the available therapies by examining their properties (Table 1). The ideal basal insulin should be long acting without identifiable peaks in concentration. For patients who are not eating, nutritional doses can be programmed with intermediate‐acting insulin. When giving insulin to patients before meals, rapid‐acting insulin analogs are best suited for the hospitalized patient because of their short onset of action. Regular insulin is also short acting, but it takes 30 minutes to take effect; thus, the dose needs to be timed at least a half hour prior to the meal. In addition, regular insulin can last for 6‐8 hours if large doses are used, which is not an ideal quality to have if trying to control postprandial glucose. The best way to mimic normal physiology is to use a combination of several types of insulin. A common strategy is to give a single daily injection of basal insulin (glargine/detimir) and then use rapid‐acting insulin analogs (lispro/aspart/glulisine) to cover prandial and correction doses.

Figure 1
Physiologic insulin requirements of healthy and sick patients.
Insulin Types
Time to Action Peak Duration
Lispro/aspart/glulisine 5‐15 minutes 1‐2 hours 3‐6 hours
Human NPH 1‐2 hours 4‐8 hours 10‐20 hours
Regular/human 30‐60 minutes 2‐4 hours 6‐10 hours
Glargine/detimir 1‐2 hours Flat 24 hours

The initial doses of scheduled subcutaneous insulin are based on previously established dose requirements, previous experience of the same patient during similar circumstances, requirements during a stable continuous insulin infusion, and/or knowledge of how stable medical condition and nutritional intake are. For patients whose insulin requirements are unknown and whose nutritional intake will be adequate, a reasonable assumption based on body weight is 0.5‐0.7 units/kg per 24 hours. Type 2 diabetics may need more, however; regardless, the patient's regimen should be started low and worked up to the dose to meet the demonstrated need. For type 1 diabetics with limited nutritional intake, the amount of scheduled insulin calculated by body weight should be reduced by 50%. For type 2 diabetics with limited nutritional intake, endogenous insulin may be adequate for basal requirements, and until results of monitoring indicate a further need for scheduled insulin, only correction doses should be used initially.

Many patients will need to transition from intravenous to subcutaneous insulin therapy when transferred from the critical care unit to the regular nursing floor. To maintain effective blood levels of insulin, it is necessary to administer short‐ or rapid‐acting insulin subcutaneously 1‐2 hours before or intermediate‐ or long‐acting insulin 2‐3 hours before stopping the insulin infusion. Subcutaneous insulin with an appropriate duration of action may be administered as a single dose or repeatedly to maintain basal effect until the time of day when insulin or analog, whichever preferred for basal effect, normally would be provided. For example, patients who typically receive glargine at night but have their insulin infusion stopped at lunchtime could receive a one‐time dose of NPH before interruption of the insulin infusion.

Hypoglycemia is a concern in hospitalized patients with diabetes, and it has been a major barrier to aggressive treatment of hyperglycemia in the hospital. Yet hypoglycemia can be predicted and prevented. Factors that increase the risk of hypoglycemia in the hospital include inadequate glucose monitoring; lack of clear communication or coordination between dietary, transportation, and nursing staff; and illegible orders.6 Clear algorithms for insulin orders and clear hypoglycemia protocols will reduce the likelihood of severe hypoglycemia occurring.

Although most positive outcomes associated with the new glycemic targets are derived from the critical care setting, there is a rationale supporting their benefit for other patients. The current glycemic targets for hospitalized patients warrant an approach that stresses the use of insulin in a way that matches normal physiology. The traditional SSI regimen is ineffective, and using it to manage glucose in the inpatient setting can no longer be justified.

Tight glycemic control in the hospitalized patient is not a simple task. Hospitalized patients are characterized by high levels of counterregulatory hormones (catecholamines, cortisol, and growth hormone) and cytokines that vary greatly in the context of sepsis, burns, hypoxia, cardiovascular disease, pain, surgery, and trauma. In addition, inpatients have unpredictable eating times and little to no physical activity. Each of the major classes of oral glycemic agents has significant limitations for inpatient use and provides little flexibility or opportunity for titration in a setting where acute changes demand these qualities. As a result, sliding‐scale insulin (SSI) regimens are often used to treat hyperglycemia in patients with or without diabetes in these clinical situations.

SSI usually consists of rapid‐acting or regular insulin ordered in a specified number of units for a given degree of hyperglycemia without regard to the timing of food, any preexisting insulin administration, or even individualization of a patient's sensitivity to insulin. This is not a physiologic approach to insulin management and not an ideal strategy for managing hyperglycemia. Because many SSI regimens do not initiate therapy until the blood glucose level is more than 200 mg/dL, SSI uses hyperglycemia as a threshold. This allows hyperglycemia to persist for long periods without intervention. In turn, SSI is reactive instead of proactive. With SSI, the current dose of insulin is based on the inadequacy of the previous dose, creating a chase‐your‐tail phenomenon. In addition, once the SSI regimen begins, glycemic control is rarely assessed by a physician until blood glucose is dangerously low or high (60 or >400 mg/dL). Finally, SSI provides no basal insulin. Hospitalized patients with stress‐induced hyperglycemia require not only postprandial insulin but also basal insulin to control blood glucose between meals and at night.

Evidence supporting SSI as a primary method of blood glucose control in diabetic patients is lacking. A search of MEDLINE for the period from 1966 to 2003 with the terms sliding scale insulin, sliding scale, and sliding combined with insulin yielded a total of 52 publications, none of which showed a benefit of sliding‐scale insulin in improving glycemic control or clinical outcomes. Retrospective and nonrandomized studies confirmed that SSI is associated with more hyper‐ and hypoglycemia with longer hospital stays.13 Queale et al. published the largest prospective cohort study (n = 171) of diabetic patients on SSI.4 More than 40% had at least one episode of hyperglycemia (>300 mg/dL), and 25% had more than one episode. Use of SSI alone increased the likelihood of hyperglycemia 3‐fold. Hypoglycemia occurred in 23%. Despite this poor performance in controlling blood glucose, the SSI remained unadjusted throughout the hospital stay for more than 80% of patients. In total, the clinical studies and clinical reviews on SSI confirmed that it is an inappropriate approach to blood glucose control in diabetic patients. Yet, SSI use in the inpatient setting continues to be a routine passed down from attending physicians to residents and medical students. In one recent study, 61% of diabetic patients admitted to the hospital for reasons other than metabolic control were on SSI.5 This sliding‐scale culture tolerates hyperglycemia and relieves the burden on the medical team to closely manage the glucose. Clinicians rely on the SSI to manage hyperglycemia rather than make frequent insulin adjustments.

Insulin, given either intravenously as a continuous infusion or subcutaneously, is the most effective agent for achieving glycemic control in hospitalized patients. Intravenous insulin infusions have been used for many years and have a proven track record for efficacy and safety. It does require frequent bedside blood glucose monitoring, which may limit its use on regular medical floors. The ideal frequency for monitoring has not been studied, but it is generally recommended that blood glucose be tested every hour until a stable infusion rate is reached. Unlike SSI, effective subcutaneous insulin therapy should define the dose components physiologically in the form of basal, nutritional or prandial, and correction doses (Fig. 1). Basal insulin is a patient's baseline level of insulin available throughout the day. Basal insulin gives the patient enough insulin to suppress hepatic glucose output, and it keeps the body from becoming hyperglycemic and ketoacidotic when not eating. Nutritional insulin is defined as the insulin needed to cover any intravenous glucose the patient is receiving, intravenous or enteral alimentation, and calories consumed in meals. If the patient is eating and is not receiving any other sources of calories, nutritional insulin would be the same as prandial insulin. In addition to basal and nutritional insulin requirements, patients often require supplemental or correction doses of insulin to treat unexpected hyperglycemia. Therefore, subcutaneous insulin can be given as a scheduled or programmed dose (basal + nutritional) and then a rapid‐acting supplemental (correction) dose to cover any hyperglycemia above target. The supplemental dose should not be confused with SSI, which does not provide any programmed basal and nutritional insulin. To provide the right amounts of basal and prandial insulin, you need to choose from the available therapies by examining their properties (Table 1). The ideal basal insulin should be long acting without identifiable peaks in concentration. For patients who are not eating, nutritional doses can be programmed with intermediate‐acting insulin. When giving insulin to patients before meals, rapid‐acting insulin analogs are best suited for the hospitalized patient because of their short onset of action. Regular insulin is also short acting, but it takes 30 minutes to take effect; thus, the dose needs to be timed at least a half hour prior to the meal. In addition, regular insulin can last for 6‐8 hours if large doses are used, which is not an ideal quality to have if trying to control postprandial glucose. The best way to mimic normal physiology is to use a combination of several types of insulin. A common strategy is to give a single daily injection of basal insulin (glargine/detimir) and then use rapid‐acting insulin analogs (lispro/aspart/glulisine) to cover prandial and correction doses.

Figure 1
Physiologic insulin requirements of healthy and sick patients.
Insulin Types
Time to Action Peak Duration
Lispro/aspart/glulisine 5‐15 minutes 1‐2 hours 3‐6 hours
Human NPH 1‐2 hours 4‐8 hours 10‐20 hours
Regular/human 30‐60 minutes 2‐4 hours 6‐10 hours
Glargine/detimir 1‐2 hours Flat 24 hours

The initial doses of scheduled subcutaneous insulin are based on previously established dose requirements, previous experience of the same patient during similar circumstances, requirements during a stable continuous insulin infusion, and/or knowledge of how stable medical condition and nutritional intake are. For patients whose insulin requirements are unknown and whose nutritional intake will be adequate, a reasonable assumption based on body weight is 0.5‐0.7 units/kg per 24 hours. Type 2 diabetics may need more, however; regardless, the patient's regimen should be started low and worked up to the dose to meet the demonstrated need. For type 1 diabetics with limited nutritional intake, the amount of scheduled insulin calculated by body weight should be reduced by 50%. For type 2 diabetics with limited nutritional intake, endogenous insulin may be adequate for basal requirements, and until results of monitoring indicate a further need for scheduled insulin, only correction doses should be used initially.

Many patients will need to transition from intravenous to subcutaneous insulin therapy when transferred from the critical care unit to the regular nursing floor. To maintain effective blood levels of insulin, it is necessary to administer short‐ or rapid‐acting insulin subcutaneously 1‐2 hours before or intermediate‐ or long‐acting insulin 2‐3 hours before stopping the insulin infusion. Subcutaneous insulin with an appropriate duration of action may be administered as a single dose or repeatedly to maintain basal effect until the time of day when insulin or analog, whichever preferred for basal effect, normally would be provided. For example, patients who typically receive glargine at night but have their insulin infusion stopped at lunchtime could receive a one‐time dose of NPH before interruption of the insulin infusion.

Hypoglycemia is a concern in hospitalized patients with diabetes, and it has been a major barrier to aggressive treatment of hyperglycemia in the hospital. Yet hypoglycemia can be predicted and prevented. Factors that increase the risk of hypoglycemia in the hospital include inadequate glucose monitoring; lack of clear communication or coordination between dietary, transportation, and nursing staff; and illegible orders.6 Clear algorithms for insulin orders and clear hypoglycemia protocols will reduce the likelihood of severe hypoglycemia occurring.

Although most positive outcomes associated with the new glycemic targets are derived from the critical care setting, there is a rationale supporting their benefit for other patients. The current glycemic targets for hospitalized patients warrant an approach that stresses the use of insulin in a way that matches normal physiology. The traditional SSI regimen is ineffective, and using it to manage glucose in the inpatient setting can no longer be justified.

References
  1. Gearhart JG,Duncan JL,Replogle WH,Forbes RC,Walley EJ.Efficacy of sliding‐scale insulin therapy: a comparison with prospective regimens.Fam Pract Res J.1994;14:313321.
  2. Smith WD,Winterstein AG,Johns T,Rosenberg E,Sauer B.Causes of hyperglycemia and hypoglycemia in adult inpatients.Am J Health Syst Pharm.2005;62:714719.
  3. Browning LA,Dumo P.Sliding‐scale insulin: an antiquated approach to glycemic control in hospitalized patients.Am J Health Syst Pharm.2004;61:16111614.
  4. Queale WS,Seidler AJ,Brancati FL.Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus.Arch Intern Med.1997;157:545552.
  5. Moghissi E.Hospital management of diabetes: beyond the sliding scale.Cleve Clin J Med.2004;71:801808.
References
  1. Gearhart JG,Duncan JL,Replogle WH,Forbes RC,Walley EJ.Efficacy of sliding‐scale insulin therapy: a comparison with prospective regimens.Fam Pract Res J.1994;14:313321.
  2. Smith WD,Winterstein AG,Johns T,Rosenberg E,Sauer B.Causes of hyperglycemia and hypoglycemia in adult inpatients.Am J Health Syst Pharm.2005;62:714719.
  3. Browning LA,Dumo P.Sliding‐scale insulin: an antiquated approach to glycemic control in hospitalized patients.Am J Health Syst Pharm.2004;61:16111614.
  4. Queale WS,Seidler AJ,Brancati FL.Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus.Arch Intern Med.1997;157:545552.
  5. Moghissi E.Hospital management of diabetes: beyond the sliding scale.Cleve Clin J Med.2004;71:801808.
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Inpatient management of diabetes: An increasing challenge to the hospitalist physician

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Inpatient management of diabetes: An increasing challenge to the hospitalist physician

In this supplement, Avoiding Complications in the Hospitalized Patient: The Case for Tight Glycemic Control, Dr. Susan S. Braithwaite defines specific populations, disorders, and hospital settings for which there now is strong evidence supporting the belief that short‐term glycemic control will affect outcomes during the course of hospital treatment.1 She provides a comprehensive summary of key studies showing the benefits of tight glycemic control in hospitalized patients. Dr. James S. Krinsley reviews the evidence that supports more intensive glucose control, along with a real‐world success story that demonstrates how to apply the new glycemic targets in a multidisciplinary performance improvement project.2 He discusses important issues surrounding the successful implementation of a tight glycemic control protocol, including barriers to implementation, setting the glycemic target, and tips for choosing the right protocol. Dr. Franklin Michota describes a practical guideline for how to implement a more physiologic and sensible insulin regimen for management of inpatient hyperglycemia.3 He reports on the disadvantages of the sliding scale and recommends the implementation of a standardized subcutaneous insulin order set with the use of scheduled basal and nutritional insulin in the inpatient management of diabetes. Drs. Asudani and Calles‐Escandon focus on the management of noncritically ill patients with hyperglycemia in medical and surgical units.4 They propose a successful insulin regimen to be used in non‐ICU settings that is based on the combined use of basal, alimentary (prandial), and corrective insulin. This supplement provides the hospitalist physician with the necessary tools to implement glycemic control programs in critical care and noncritical care units and can be summarized as follows.

Hyperglycemia in hospitalized patients is a common, serious, and costly health care problem with profound medical consequences. Thirty‐eight percent of patients admitted to the hospital have hyperglycemia, about one third of whom have no history of diabetes before admission.5 Increasing evidence indicates that the development of hyperglycemia during acute medical or surgical illness is not a physiologic or benign condition but is a marker of poor clinical outcome and mortality.510 Evidence from observational studies indicates that the development of hyperglycemia in critical illness is associated with an increased risk of complications and mortality, a longer hospital stay, a higher rate of admission to the ICU, and a higher likelihood that transitional or nursing home care after hospital discharge will be required.5, 7, 914 Prospective randomized trials with critical care patients have shown that aggressive glycemic control reduces short‐ and long‐term mortality, multiorgan failure, systemic infections, and length of hospital and ICU stays7, 911 and lower the total cost of hospitalization.15 Controlling hyperglycemia is also important for adult patients admitted to general surgical and medical wards. In such patients, the presence of hyperglycemia is associated with prolonged hospital stay, infection, disability after hospital discharge, and death.5, 11, 16

Insulin, given either intravenously as a continuous infusion or subcutaneously, is currently the only available agent for effectively controlling glycemia in the hospital. In the critical care setting, a variety of intravenous infusion protocols have been shown to be effective in achieving glycemic control with a low‐rate of hypoglycemic events and in improving hospital outcomes.1723 However, no prospective and randomized interventional studies have focused on the optimal management of hyperglycemia and its effect on clinical outcome among noncritically ill patients admitted to general medicine services. Fear of hypoglycemia leads physicians to inappropriately hold to their patients' previous outpatient diabetic regimens and to initiate sliding‐scale insulin coverage, a practice associated with limited therapeutic success.20, 24, 25 The most physiologic and effective insulin therapy provides both basal and nutritional insulin.11 The basal insulin requirement is the amount of exogenous insulin necessary to regulate hepatic glucose production and peripheral glucose uptake and to prevent ketogenesis. The nutritional, or prandial, insulin requirement is the amount of insulin necessary to cover meals and the administration of intravenous dextrose, TPN, and enteral feedings. Prandial or mealtime insulin replacement has its main effect on peripheral glucose disposal. In addition to the basal and nutritional insulin requirements, patients often require supplemental or correction doses of insulin to treat unexpected hyperglycemia. The supplemental algorithm should not be confused with the sliding scale, which traditionally has been used alone, with no scheduled dose. Insulins used for basal requirements are NPH (which is intermediate acting) and long‐acting insulin analogues (glargine and detemir). To cover nutritional need, regular insulin or rapid‐acting analogues (lispro, aspart, glulisine) can be used. Although no inpatient controlled trials using the basal‐nutritional insulin regimen have been reported, the use of basal and nutritional insulin regimen may be a better alternative to the use of intermediate insulin (NPH) and regular insulin in hospitalized patients.

Hypoglycemia in hospitalized patients with diabetes is a concern, and it has been a major barrier to aggressive treatment of hyperglycemia in the hospital. Severe hypoglycemia, defined as a glucose level less than 40 mg/dL, occurred at least once in 5.1% of patients in the intensively treated group in Van den Berghe's surgical ICU study, versus 0.8% of patients in the conventionally treated group.19 The incidence of severe hypoglycemia (40 mg/dL) reported by Krinsley et al. prior to institution of the intensified protocol was 0.35% of all values obtained, compared to 0.34% of those obtained during the treatment period, again without any overt adverse consequences.26 Factors that increase the risk of hypoglycemia in the hospital include inadequate glucose monitoring, lack of clear communication or coordination between the dietary team, transportation, and nursing staff, and indecipherable orders. Clear algorithms for insulin orders and clear hypoglycemia protocols are critical to preventing hypoglycemia.

What should the target blood glucose level be in noncritically ill patients with diabetes? A recent position statement of the American Association of Clinical Endocrinology with cosponsorship by the American Diabetes Association, the American Heart Association, the American Society of Anesthesiologists, the Endocrine Society, the Society of Critical Care Medicine, the Society of Hospital Medicine, the Society of Thoracic Surgeons, and the American Association of Diabetes Educators27 recommended a glycemic target between 80 and 110 mg/dL for hospitalized patients in the intensive care unit and a preprandial glucose goal of less than 110 mg/dL and a random glucose less than 180 mg/dL for patients in noncritical care settings. The Joint Commission on Accreditation of Healthcare Organization recently proposed tight glucose control for the critically ill as a core quality of care measure for all U.S. hospitals that participate in the Medicare program (www.jcaho.org). Recently, some experts have endorsed a more conservative blood glucose value, up to 140 mg/dL26, 28 or even higher, if the patient is not in a critical care unit. Until clinical recommendations supported by prospective randomized trials become available, it is prudent to approach management of hospitalized patients with caution, but with the understanding that any blood glucose threshold greater than 140 mg/dL in the ICU and greater than 180 mg/dL in noncritical care areas should be avoided.

References
  1. Braithwaite SB.Defining the benefits of euglycemia in the hospitalized patient.J Hosp Med.2007;2(suppl 1):512.
  2. Krinsley J.Translating evidence into practice in managing inpatient hyperglycemia.J Hosp Med.2007;2(suppl 1):1319.
  3. Michota F.What are the disadvantages of sliding‐scale insulin?J Hosp Med.2007;2(suppl 1):2022.
  4. Asudani D,Calles‐Escandon J.Inpatient hyperglycemia: Slide through the scale but cover the bases first.J Hosp Med.2007;2(suppl 1):2332.
  5. Umpierrez GE,Isaacs SD,Bazargan N,You X,Thaler LM,Kitabchi AE.Hyperglycemia: an independent marker of in‐hospital mortality in patients with undiagnosed diabetes.J Clin Endocrinol Metab.2002;87:978982.
  6. Capes SE,Hunt D,Malmberg K,Gerstein HC.Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview.Lancet2000;355:773778.
  7. Finney SJ,Zekveld C,Elia A,Evans TW:Glucose control and mortality in critically ill patients.JAMA.2003;290:20412047.
  8. Levetan CS,Magee MF:Hospital management of diabetes.Endocrinol Metab Clin North Am.2000;29:745770.
  9. Wahab NN,Cowden EA,Pearce NJ,Gardner MJ,Merry H,Cox JL.Is blood glucose an independent predictor of mortality in acute myocardial infarction in the thrombolytic era?J Am Coll Cardiol.2002;40:17481754.
  10. Norhammar AM,Ryden L,Malmberg K.Admission plasma glucose. Independent risk factor for long‐term prognosis after myocardial infarction even in nondiabetic patients.Diabetes Care.1999;22:18271831.
  11. Clement S,Braithwaite SS,Magee MF,Ahmann A,Smith EP,Schafer RG,Hirsh IB.Management of diabetes and hyperglycemia in hospitals.Diabetes Care.27:553597,2004
  12. Montori VM,Bistrian BR,McMahon MM.Hyperglycemia in acutely ill patients.JAMA.2002;288:21672169.
  13. Stranders I,Diamant M,van Gelder RE,Spruijt HJ,Twisk JW,Heine RJ,Visser FC.Admission blood glucose level as risk indicator of death after myocardial infarction in patients with and without diabetes mellitus.Arch Intern Med.2004;164:982988.
  14. Umpierrez GE,A EK.ICU care for patients with diabetes.Current Opinions Endocrinol.2004;11:7581.
  15. Krinsley JS,Jones RL.Cost analysis of intensive glycemic control in critically ill adult patients.Chest.2006;129:644650.
  16. Pomposelli JJ,Baxter JK,Babineau TJ, et al.Early postoperative glucose control predicts nosocomial infection rate in diabetic patients.JPEN J Parenter Enteral Nutr.1998;22:7781.
  17. Malmberg KA,Efendic S,Ryden LE:Feasibility of insulin‐glucose infusion in diabetic patients with acute myocardial infarction. A report from the multicenter trial: DIGAMI.Diabetes Care.1994;17:10071014.
  18. Umpierrez GE,Kelly JP,Navarrete JE,Casals MM,Kitabchi AE.Hyperglycemic crises in urban blacks.Arch Intern Med.1997;157:669675.
  19. van den Berghe G,Wouters P,Weekers F, et al.Intensive insulin therapy in the critically ill patients.N Engl J Med.2001;345:13591367.
  20. Brown G,Dodek P.Intravenous insulin nomogram improves blood glucose control in the critically ill.Crit Care Med.2001;29:17141719.
  21. Furnary AP,Gao G,Grunkemeier GL, et al.Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting.J Thorac Cardiovasc Surg.2003;125:10071021.
  22. Furnary AP,Zerr KJ,Grunkemeier GL,Starr A.Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures.Ann Thorac Surg.1999;67:352360; discussion360352.
  23. Goldberg PA,Siegel MD,Sherwin RS, et al.Implementation of a safe and effective insulin infusion protocol in a medical intensive care unit.Diabetes Care.2004;27:461467.
  24. Queale WS,Seidler AJ,Brancati FL.Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus.Arch Intern Med.1997;157:545552.
  25. Gearhart JG,Duncan JL,Replogle WH,Forbes RC,Walley EJ.Efficacy of sliding‐scale insulin therapy: a comparison with prospective regimens.Fam Pract Res J.1994;14:313322.
  26. Krinsley JS.Association between hyperglycemia and increased hospital mortality in a heterogeneous population of critically ill patients.Mayo Clin Proc.2003;78:14711478.
  27. Garber AJ,Moghissi ES,Bransome ED, et al.American College of Endocrinology position statement on inpatient diabetes and metabolic control.Endocr Pract.2004;10(suppl 2):49.
  28. Inzucchi SE,Rosenstock J.Counterpoint: inpatient glucose management: a premature call to arms?Diabetes Care.2005;28:976979.
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In this supplement, Avoiding Complications in the Hospitalized Patient: The Case for Tight Glycemic Control, Dr. Susan S. Braithwaite defines specific populations, disorders, and hospital settings for which there now is strong evidence supporting the belief that short‐term glycemic control will affect outcomes during the course of hospital treatment.1 She provides a comprehensive summary of key studies showing the benefits of tight glycemic control in hospitalized patients. Dr. James S. Krinsley reviews the evidence that supports more intensive glucose control, along with a real‐world success story that demonstrates how to apply the new glycemic targets in a multidisciplinary performance improvement project.2 He discusses important issues surrounding the successful implementation of a tight glycemic control protocol, including barriers to implementation, setting the glycemic target, and tips for choosing the right protocol. Dr. Franklin Michota describes a practical guideline for how to implement a more physiologic and sensible insulin regimen for management of inpatient hyperglycemia.3 He reports on the disadvantages of the sliding scale and recommends the implementation of a standardized subcutaneous insulin order set with the use of scheduled basal and nutritional insulin in the inpatient management of diabetes. Drs. Asudani and Calles‐Escandon focus on the management of noncritically ill patients with hyperglycemia in medical and surgical units.4 They propose a successful insulin regimen to be used in non‐ICU settings that is based on the combined use of basal, alimentary (prandial), and corrective insulin. This supplement provides the hospitalist physician with the necessary tools to implement glycemic control programs in critical care and noncritical care units and can be summarized as follows.

Hyperglycemia in hospitalized patients is a common, serious, and costly health care problem with profound medical consequences. Thirty‐eight percent of patients admitted to the hospital have hyperglycemia, about one third of whom have no history of diabetes before admission.5 Increasing evidence indicates that the development of hyperglycemia during acute medical or surgical illness is not a physiologic or benign condition but is a marker of poor clinical outcome and mortality.510 Evidence from observational studies indicates that the development of hyperglycemia in critical illness is associated with an increased risk of complications and mortality, a longer hospital stay, a higher rate of admission to the ICU, and a higher likelihood that transitional or nursing home care after hospital discharge will be required.5, 7, 914 Prospective randomized trials with critical care patients have shown that aggressive glycemic control reduces short‐ and long‐term mortality, multiorgan failure, systemic infections, and length of hospital and ICU stays7, 911 and lower the total cost of hospitalization.15 Controlling hyperglycemia is also important for adult patients admitted to general surgical and medical wards. In such patients, the presence of hyperglycemia is associated with prolonged hospital stay, infection, disability after hospital discharge, and death.5, 11, 16

Insulin, given either intravenously as a continuous infusion or subcutaneously, is currently the only available agent for effectively controlling glycemia in the hospital. In the critical care setting, a variety of intravenous infusion protocols have been shown to be effective in achieving glycemic control with a low‐rate of hypoglycemic events and in improving hospital outcomes.1723 However, no prospective and randomized interventional studies have focused on the optimal management of hyperglycemia and its effect on clinical outcome among noncritically ill patients admitted to general medicine services. Fear of hypoglycemia leads physicians to inappropriately hold to their patients' previous outpatient diabetic regimens and to initiate sliding‐scale insulin coverage, a practice associated with limited therapeutic success.20, 24, 25 The most physiologic and effective insulin therapy provides both basal and nutritional insulin.11 The basal insulin requirement is the amount of exogenous insulin necessary to regulate hepatic glucose production and peripheral glucose uptake and to prevent ketogenesis. The nutritional, or prandial, insulin requirement is the amount of insulin necessary to cover meals and the administration of intravenous dextrose, TPN, and enteral feedings. Prandial or mealtime insulin replacement has its main effect on peripheral glucose disposal. In addition to the basal and nutritional insulin requirements, patients often require supplemental or correction doses of insulin to treat unexpected hyperglycemia. The supplemental algorithm should not be confused with the sliding scale, which traditionally has been used alone, with no scheduled dose. Insulins used for basal requirements are NPH (which is intermediate acting) and long‐acting insulin analogues (glargine and detemir). To cover nutritional need, regular insulin or rapid‐acting analogues (lispro, aspart, glulisine) can be used. Although no inpatient controlled trials using the basal‐nutritional insulin regimen have been reported, the use of basal and nutritional insulin regimen may be a better alternative to the use of intermediate insulin (NPH) and regular insulin in hospitalized patients.

Hypoglycemia in hospitalized patients with diabetes is a concern, and it has been a major barrier to aggressive treatment of hyperglycemia in the hospital. Severe hypoglycemia, defined as a glucose level less than 40 mg/dL, occurred at least once in 5.1% of patients in the intensively treated group in Van den Berghe's surgical ICU study, versus 0.8% of patients in the conventionally treated group.19 The incidence of severe hypoglycemia (40 mg/dL) reported by Krinsley et al. prior to institution of the intensified protocol was 0.35% of all values obtained, compared to 0.34% of those obtained during the treatment period, again without any overt adverse consequences.26 Factors that increase the risk of hypoglycemia in the hospital include inadequate glucose monitoring, lack of clear communication or coordination between the dietary team, transportation, and nursing staff, and indecipherable orders. Clear algorithms for insulin orders and clear hypoglycemia protocols are critical to preventing hypoglycemia.

What should the target blood glucose level be in noncritically ill patients with diabetes? A recent position statement of the American Association of Clinical Endocrinology with cosponsorship by the American Diabetes Association, the American Heart Association, the American Society of Anesthesiologists, the Endocrine Society, the Society of Critical Care Medicine, the Society of Hospital Medicine, the Society of Thoracic Surgeons, and the American Association of Diabetes Educators27 recommended a glycemic target between 80 and 110 mg/dL for hospitalized patients in the intensive care unit and a preprandial glucose goal of less than 110 mg/dL and a random glucose less than 180 mg/dL for patients in noncritical care settings. The Joint Commission on Accreditation of Healthcare Organization recently proposed tight glucose control for the critically ill as a core quality of care measure for all U.S. hospitals that participate in the Medicare program (www.jcaho.org). Recently, some experts have endorsed a more conservative blood glucose value, up to 140 mg/dL26, 28 or even higher, if the patient is not in a critical care unit. Until clinical recommendations supported by prospective randomized trials become available, it is prudent to approach management of hospitalized patients with caution, but with the understanding that any blood glucose threshold greater than 140 mg/dL in the ICU and greater than 180 mg/dL in noncritical care areas should be avoided.

In this supplement, Avoiding Complications in the Hospitalized Patient: The Case for Tight Glycemic Control, Dr. Susan S. Braithwaite defines specific populations, disorders, and hospital settings for which there now is strong evidence supporting the belief that short‐term glycemic control will affect outcomes during the course of hospital treatment.1 She provides a comprehensive summary of key studies showing the benefits of tight glycemic control in hospitalized patients. Dr. James S. Krinsley reviews the evidence that supports more intensive glucose control, along with a real‐world success story that demonstrates how to apply the new glycemic targets in a multidisciplinary performance improvement project.2 He discusses important issues surrounding the successful implementation of a tight glycemic control protocol, including barriers to implementation, setting the glycemic target, and tips for choosing the right protocol. Dr. Franklin Michota describes a practical guideline for how to implement a more physiologic and sensible insulin regimen for management of inpatient hyperglycemia.3 He reports on the disadvantages of the sliding scale and recommends the implementation of a standardized subcutaneous insulin order set with the use of scheduled basal and nutritional insulin in the inpatient management of diabetes. Drs. Asudani and Calles‐Escandon focus on the management of noncritically ill patients with hyperglycemia in medical and surgical units.4 They propose a successful insulin regimen to be used in non‐ICU settings that is based on the combined use of basal, alimentary (prandial), and corrective insulin. This supplement provides the hospitalist physician with the necessary tools to implement glycemic control programs in critical care and noncritical care units and can be summarized as follows.

Hyperglycemia in hospitalized patients is a common, serious, and costly health care problem with profound medical consequences. Thirty‐eight percent of patients admitted to the hospital have hyperglycemia, about one third of whom have no history of diabetes before admission.5 Increasing evidence indicates that the development of hyperglycemia during acute medical or surgical illness is not a physiologic or benign condition but is a marker of poor clinical outcome and mortality.510 Evidence from observational studies indicates that the development of hyperglycemia in critical illness is associated with an increased risk of complications and mortality, a longer hospital stay, a higher rate of admission to the ICU, and a higher likelihood that transitional or nursing home care after hospital discharge will be required.5, 7, 914 Prospective randomized trials with critical care patients have shown that aggressive glycemic control reduces short‐ and long‐term mortality, multiorgan failure, systemic infections, and length of hospital and ICU stays7, 911 and lower the total cost of hospitalization.15 Controlling hyperglycemia is also important for adult patients admitted to general surgical and medical wards. In such patients, the presence of hyperglycemia is associated with prolonged hospital stay, infection, disability after hospital discharge, and death.5, 11, 16

Insulin, given either intravenously as a continuous infusion or subcutaneously, is currently the only available agent for effectively controlling glycemia in the hospital. In the critical care setting, a variety of intravenous infusion protocols have been shown to be effective in achieving glycemic control with a low‐rate of hypoglycemic events and in improving hospital outcomes.1723 However, no prospective and randomized interventional studies have focused on the optimal management of hyperglycemia and its effect on clinical outcome among noncritically ill patients admitted to general medicine services. Fear of hypoglycemia leads physicians to inappropriately hold to their patients' previous outpatient diabetic regimens and to initiate sliding‐scale insulin coverage, a practice associated with limited therapeutic success.20, 24, 25 The most physiologic and effective insulin therapy provides both basal and nutritional insulin.11 The basal insulin requirement is the amount of exogenous insulin necessary to regulate hepatic glucose production and peripheral glucose uptake and to prevent ketogenesis. The nutritional, or prandial, insulin requirement is the amount of insulin necessary to cover meals and the administration of intravenous dextrose, TPN, and enteral feedings. Prandial or mealtime insulin replacement has its main effect on peripheral glucose disposal. In addition to the basal and nutritional insulin requirements, patients often require supplemental or correction doses of insulin to treat unexpected hyperglycemia. The supplemental algorithm should not be confused with the sliding scale, which traditionally has been used alone, with no scheduled dose. Insulins used for basal requirements are NPH (which is intermediate acting) and long‐acting insulin analogues (glargine and detemir). To cover nutritional need, regular insulin or rapid‐acting analogues (lispro, aspart, glulisine) can be used. Although no inpatient controlled trials using the basal‐nutritional insulin regimen have been reported, the use of basal and nutritional insulin regimen may be a better alternative to the use of intermediate insulin (NPH) and regular insulin in hospitalized patients.

Hypoglycemia in hospitalized patients with diabetes is a concern, and it has been a major barrier to aggressive treatment of hyperglycemia in the hospital. Severe hypoglycemia, defined as a glucose level less than 40 mg/dL, occurred at least once in 5.1% of patients in the intensively treated group in Van den Berghe's surgical ICU study, versus 0.8% of patients in the conventionally treated group.19 The incidence of severe hypoglycemia (40 mg/dL) reported by Krinsley et al. prior to institution of the intensified protocol was 0.35% of all values obtained, compared to 0.34% of those obtained during the treatment period, again without any overt adverse consequences.26 Factors that increase the risk of hypoglycemia in the hospital include inadequate glucose monitoring, lack of clear communication or coordination between the dietary team, transportation, and nursing staff, and indecipherable orders. Clear algorithms for insulin orders and clear hypoglycemia protocols are critical to preventing hypoglycemia.

What should the target blood glucose level be in noncritically ill patients with diabetes? A recent position statement of the American Association of Clinical Endocrinology with cosponsorship by the American Diabetes Association, the American Heart Association, the American Society of Anesthesiologists, the Endocrine Society, the Society of Critical Care Medicine, the Society of Hospital Medicine, the Society of Thoracic Surgeons, and the American Association of Diabetes Educators27 recommended a glycemic target between 80 and 110 mg/dL for hospitalized patients in the intensive care unit and a preprandial glucose goal of less than 110 mg/dL and a random glucose less than 180 mg/dL for patients in noncritical care settings. The Joint Commission on Accreditation of Healthcare Organization recently proposed tight glucose control for the critically ill as a core quality of care measure for all U.S. hospitals that participate in the Medicare program (www.jcaho.org). Recently, some experts have endorsed a more conservative blood glucose value, up to 140 mg/dL26, 28 or even higher, if the patient is not in a critical care unit. Until clinical recommendations supported by prospective randomized trials become available, it is prudent to approach management of hospitalized patients with caution, but with the understanding that any blood glucose threshold greater than 140 mg/dL in the ICU and greater than 180 mg/dL in noncritical care areas should be avoided.

References
  1. Braithwaite SB.Defining the benefits of euglycemia in the hospitalized patient.J Hosp Med.2007;2(suppl 1):512.
  2. Krinsley J.Translating evidence into practice in managing inpatient hyperglycemia.J Hosp Med.2007;2(suppl 1):1319.
  3. Michota F.What are the disadvantages of sliding‐scale insulin?J Hosp Med.2007;2(suppl 1):2022.
  4. Asudani D,Calles‐Escandon J.Inpatient hyperglycemia: Slide through the scale but cover the bases first.J Hosp Med.2007;2(suppl 1):2332.
  5. Umpierrez GE,Isaacs SD,Bazargan N,You X,Thaler LM,Kitabchi AE.Hyperglycemia: an independent marker of in‐hospital mortality in patients with undiagnosed diabetes.J Clin Endocrinol Metab.2002;87:978982.
  6. Capes SE,Hunt D,Malmberg K,Gerstein HC.Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview.Lancet2000;355:773778.
  7. Finney SJ,Zekveld C,Elia A,Evans TW:Glucose control and mortality in critically ill patients.JAMA.2003;290:20412047.
  8. Levetan CS,Magee MF:Hospital management of diabetes.Endocrinol Metab Clin North Am.2000;29:745770.
  9. Wahab NN,Cowden EA,Pearce NJ,Gardner MJ,Merry H,Cox JL.Is blood glucose an independent predictor of mortality in acute myocardial infarction in the thrombolytic era?J Am Coll Cardiol.2002;40:17481754.
  10. Norhammar AM,Ryden L,Malmberg K.Admission plasma glucose. Independent risk factor for long‐term prognosis after myocardial infarction even in nondiabetic patients.Diabetes Care.1999;22:18271831.
  11. Clement S,Braithwaite SS,Magee MF,Ahmann A,Smith EP,Schafer RG,Hirsh IB.Management of diabetes and hyperglycemia in hospitals.Diabetes Care.27:553597,2004
  12. Montori VM,Bistrian BR,McMahon MM.Hyperglycemia in acutely ill patients.JAMA.2002;288:21672169.
  13. Stranders I,Diamant M,van Gelder RE,Spruijt HJ,Twisk JW,Heine RJ,Visser FC.Admission blood glucose level as risk indicator of death after myocardial infarction in patients with and without diabetes mellitus.Arch Intern Med.2004;164:982988.
  14. Umpierrez GE,A EK.ICU care for patients with diabetes.Current Opinions Endocrinol.2004;11:7581.
  15. Krinsley JS,Jones RL.Cost analysis of intensive glycemic control in critically ill adult patients.Chest.2006;129:644650.
  16. Pomposelli JJ,Baxter JK,Babineau TJ, et al.Early postoperative glucose control predicts nosocomial infection rate in diabetic patients.JPEN J Parenter Enteral Nutr.1998;22:7781.
  17. Malmberg KA,Efendic S,Ryden LE:Feasibility of insulin‐glucose infusion in diabetic patients with acute myocardial infarction. A report from the multicenter trial: DIGAMI.Diabetes Care.1994;17:10071014.
  18. Umpierrez GE,Kelly JP,Navarrete JE,Casals MM,Kitabchi AE.Hyperglycemic crises in urban blacks.Arch Intern Med.1997;157:669675.
  19. van den Berghe G,Wouters P,Weekers F, et al.Intensive insulin therapy in the critically ill patients.N Engl J Med.2001;345:13591367.
  20. Brown G,Dodek P.Intravenous insulin nomogram improves blood glucose control in the critically ill.Crit Care Med.2001;29:17141719.
  21. Furnary AP,Gao G,Grunkemeier GL, et al.Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting.J Thorac Cardiovasc Surg.2003;125:10071021.
  22. Furnary AP,Zerr KJ,Grunkemeier GL,Starr A.Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures.Ann Thorac Surg.1999;67:352360; discussion360352.
  23. Goldberg PA,Siegel MD,Sherwin RS, et al.Implementation of a safe and effective insulin infusion protocol in a medical intensive care unit.Diabetes Care.2004;27:461467.
  24. Queale WS,Seidler AJ,Brancati FL.Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus.Arch Intern Med.1997;157:545552.
  25. Gearhart JG,Duncan JL,Replogle WH,Forbes RC,Walley EJ.Efficacy of sliding‐scale insulin therapy: a comparison with prospective regimens.Fam Pract Res J.1994;14:313322.
  26. Krinsley JS.Association between hyperglycemia and increased hospital mortality in a heterogeneous population of critically ill patients.Mayo Clin Proc.2003;78:14711478.
  27. Garber AJ,Moghissi ES,Bransome ED, et al.American College of Endocrinology position statement on inpatient diabetes and metabolic control.Endocr Pract.2004;10(suppl 2):49.
  28. Inzucchi SE,Rosenstock J.Counterpoint: inpatient glucose management: a premature call to arms?Diabetes Care.2005;28:976979.
References
  1. Braithwaite SB.Defining the benefits of euglycemia in the hospitalized patient.J Hosp Med.2007;2(suppl 1):512.
  2. Krinsley J.Translating evidence into practice in managing inpatient hyperglycemia.J Hosp Med.2007;2(suppl 1):1319.
  3. Michota F.What are the disadvantages of sliding‐scale insulin?J Hosp Med.2007;2(suppl 1):2022.
  4. Asudani D,Calles‐Escandon J.Inpatient hyperglycemia: Slide through the scale but cover the bases first.J Hosp Med.2007;2(suppl 1):2332.
  5. Umpierrez GE,Isaacs SD,Bazargan N,You X,Thaler LM,Kitabchi AE.Hyperglycemia: an independent marker of in‐hospital mortality in patients with undiagnosed diabetes.J Clin Endocrinol Metab.2002;87:978982.
  6. Capes SE,Hunt D,Malmberg K,Gerstein HC.Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview.Lancet2000;355:773778.
  7. Finney SJ,Zekveld C,Elia A,Evans TW:Glucose control and mortality in critically ill patients.JAMA.2003;290:20412047.
  8. Levetan CS,Magee MF:Hospital management of diabetes.Endocrinol Metab Clin North Am.2000;29:745770.
  9. Wahab NN,Cowden EA,Pearce NJ,Gardner MJ,Merry H,Cox JL.Is blood glucose an independent predictor of mortality in acute myocardial infarction in the thrombolytic era?J Am Coll Cardiol.2002;40:17481754.
  10. Norhammar AM,Ryden L,Malmberg K.Admission plasma glucose. Independent risk factor for long‐term prognosis after myocardial infarction even in nondiabetic patients.Diabetes Care.1999;22:18271831.
  11. Clement S,Braithwaite SS,Magee MF,Ahmann A,Smith EP,Schafer RG,Hirsh IB.Management of diabetes and hyperglycemia in hospitals.Diabetes Care.27:553597,2004
  12. Montori VM,Bistrian BR,McMahon MM.Hyperglycemia in acutely ill patients.JAMA.2002;288:21672169.
  13. Stranders I,Diamant M,van Gelder RE,Spruijt HJ,Twisk JW,Heine RJ,Visser FC.Admission blood glucose level as risk indicator of death after myocardial infarction in patients with and without diabetes mellitus.Arch Intern Med.2004;164:982988.
  14. Umpierrez GE,A EK.ICU care for patients with diabetes.Current Opinions Endocrinol.2004;11:7581.
  15. Krinsley JS,Jones RL.Cost analysis of intensive glycemic control in critically ill adult patients.Chest.2006;129:644650.
  16. Pomposelli JJ,Baxter JK,Babineau TJ, et al.Early postoperative glucose control predicts nosocomial infection rate in diabetic patients.JPEN J Parenter Enteral Nutr.1998;22:7781.
  17. Malmberg KA,Efendic S,Ryden LE:Feasibility of insulin‐glucose infusion in diabetic patients with acute myocardial infarction. A report from the multicenter trial: DIGAMI.Diabetes Care.1994;17:10071014.
  18. Umpierrez GE,Kelly JP,Navarrete JE,Casals MM,Kitabchi AE.Hyperglycemic crises in urban blacks.Arch Intern Med.1997;157:669675.
  19. van den Berghe G,Wouters P,Weekers F, et al.Intensive insulin therapy in the critically ill patients.N Engl J Med.2001;345:13591367.
  20. Brown G,Dodek P.Intravenous insulin nomogram improves blood glucose control in the critically ill.Crit Care Med.2001;29:17141719.
  21. Furnary AP,Gao G,Grunkemeier GL, et al.Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting.J Thorac Cardiovasc Surg.2003;125:10071021.
  22. Furnary AP,Zerr KJ,Grunkemeier GL,Starr A.Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures.Ann Thorac Surg.1999;67:352360; discussion360352.
  23. Goldberg PA,Siegel MD,Sherwin RS, et al.Implementation of a safe and effective insulin infusion protocol in a medical intensive care unit.Diabetes Care.2004;27:461467.
  24. Queale WS,Seidler AJ,Brancati FL.Glycemic control and sliding scale insulin use in medical inpatients with diabetes mellitus.Arch Intern Med.1997;157:545552.
  25. Gearhart JG,Duncan JL,Replogle WH,Forbes RC,Walley EJ.Efficacy of sliding‐scale insulin therapy: a comparison with prospective regimens.Fam Pract Res J.1994;14:313322.
  26. Krinsley JS.Association between hyperglycemia and increased hospital mortality in a heterogeneous population of critically ill patients.Mayo Clin Proc.2003;78:14711478.
  27. Garber AJ,Moghissi ES,Bransome ED, et al.American College of Endocrinology position statement on inpatient diabetes and metabolic control.Endocr Pract.2004;10(suppl 2):49.
  28. Inzucchi SE,Rosenstock J.Counterpoint: inpatient glucose management: a premature call to arms?Diabetes Care.2005;28:976979.
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