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This Month's CME Article in Clinical Geriatrics

The Role and Utility of BNP in Older Patients with Heart Failure
Bibban Bant K. Deol, MD, Peter V. Vaitkevicius, MD, and Lavoisier J. Cardozo, MD

Despite advances in management and therapies, heart failure (HF) remains a major health and economic concern in the United States and around the world. Currently, there are approximately 5.3 million people with HF, with approximately 550,000 new cases diagnosed annually. There has been a significant increase of nearly 171% in the number of patients discharged from hospitals with the diagnosis of HF. Additionally, for 2008, the direct and indirect costs of HF in the United States is estimated to be $34.8 billion.

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Feature Article

Postoperative Management of Diabetes Mellitus

Postoperative Management of Diabetes Mellitus

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Dr. Hoogwerf is a staff physician, Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic Foundation, Cleveland, OH. Postoperative management of diabetes mellitus requires an understanding of disease type, the variables that affect hyperglycemia in the perioperative period, the management strategies for hyperglycemia, and the impact of disease complications. Patients should be instructed on the importance of diet, glycemic control, and management of hypertension, dyslipidemia, and aspirin use, as well as basic guidelines for foot care. Treatment regimens need to be carefully individualized in patients with diabetes following the surgical procedure.(Annals of Long-Term Care: Clinical Care and Aging 2003;11[12]:34-40) Diabetes mellitus (DM) is broadly classified as type 1 (an insulinopenic form), type 2 (an insulin-resistant form with varying degrees of insulinopenia), secondary (eg, due to glucocorticoid administration, Cushing’s syndrome, hemochromatosis, or pancreatectomy), or gestational diabetes (GDM; first diagnosed during pregnancy and usually remits after pregnancy). Persons with type 1 diabetes comprise approximately 10% of the population with diabetes.1 These patients develop hyperglycemia as a result of a loss of beta cell function and need insulin for glucose management. Those with type 2 diabetes, who comprise the remaining percentage, develop hyperglycemia as a result of insulin resistance (often associated with obesity), increased hepatic glucose production, and varying degrees of relative or absolute insulinopenia. Secondary forms of DM may mimic features of type 1 diabetes if they result from insulinopenia (eg, pancreatectomy) or type 2 diabetes if they result from insulin resistance (eg, endogenous/exogenous glucocorticoids). GDM is most closely related to type 2 DM. Therefore, for this discussion, only issues related to the management of type 1 and type 2 DM will be discussed.

GLYCEMIC CONTROL IN THE PERIOPERATIVE STATE Numerous variables affect glucose control in the postoperative period. Most important are nutrient intake and the type and dose of antihyperglycemic medications. Nutrient intake in the form of intravenous (IV) fluids and oral nutrients is often widely variable in the postoperative state. Stress hormone levels in the postoperative state predispose to hyperglycemia. Changes in activity level, infection, and some medications may also increase risk for hyperglycemia. Each must be considered in the perioperative management of the individual with this condition. In addition, pharmacologic therapy used to control hyperglycemia (oral glucose-lowering agents and/or insulin) prior to surgery should influence decisions regarding perioperative glucose management. Adequate postoperative glycemic control is important in persons with diabetes to improve wound healing, reduce the risk for wound infections, and possibly improve overall outcomes, including reduced mortality.2-7 The importance of chronic glycemic control for prevention of vascular complications of diabetes is now well established.8-14 Maintaining reasonable glycemic control in the hospitalized population helps reinforce the importance of chronic glycemic control for the patient.

COMPLICATIONS AND CONSIDERATIONS The four classic complications of DM are diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, and atherosclerotic vascular disease, including coronary heart disease, stroke, and peripheral vascular disease. Each may influence perioperative course and management. Atherosclerotic vascular disease in the patient with diabetes is associated with increased risk and increased morbidity/mortality for postsurgical myocardial infarction, stroke, or peripheral vascular disease. Since ischemic heart disease may be "silent" in patients with diabetes, situations that may aggravate myocardial ischemia in the postoperative state, such as hypotension or fever (with associated increased cardiac output) always raise special concerns in this population. Diabetic peripheral neuropathy is commonly associated with insensate feet--a predisposing cause for foot ulcers in those with DM.15,16 Proper footwear, especially heel protection while in bed, is especially important in postoperative patients. When associated lower-extremity atherosclerotic occlusive disease exists, not only is there increased risk for lower-extremity ulcers, but such pressure ulcers are also more difficult to treat. This is a serious postoperative complication that increases morbidity and length of hospital stay. Diabetic autonomic neuropathy has several potential adverse effects in the postoperative state. These include diminished bladder tone (and the associated increased risk for urinary retention), gastropathy or gastroparesis (which may be aggravated by narcotic analgesics, thereby delaying the capacity for oral nutritional intake), and sometimes increased risk for orthostatic hypotension with early postoperative ambulation. Diabetic nephropathy may be associated with mild evidence of renal compromise. This underlying impairment of renal function may be complicated by loss of renal function from postoperative hypotension (resulting in acute tubular necrosis) or medication toxicity (eg, aminoglycosides, or administration of radiocontrast). These acute insults superimposed on chronic renal impairment increase the likelihood of needing dialysis support. Diabetic retinopathy is a common cause of visual impairment. This loss of visual acuity may impair functions important to postoperative recovery, including ambulation and ability to read menus and/or instruction sheets, and can lead to increased risk of postoperative confusion or delirium. Postoperative management of the patient with DM must include considerations of disease type, the importance of glycemic control, and concerns about reducing the risk for complications of surgery because of associated comorbid conditions. Several recent articles17-23 on the management of patients with DM who are undergoing surgery afford additional insights into these issues.

GLYCEMIC CONTROL Preoperative The best outcomes in the postoperative state are achieved if efforts at glycemic control are considered in the preoperative period. The evidence that rigorous glycemic control in the immediate preoperative state has a significant impact on surgical outcomes is limited. Nevertheless, most clinicians believe that achieving modest glycemic control is worthwhile. In addition, postoperative management strategies are partially dependent on the nature of the preoperative glucose control regimen. Patients managed with diet and exercise alone may not need any additional medications for preoperative glycemic control. If evidence of acute decompensation of glucose levels is present because of medications or underlying disease (eg, infections), some preoperative insulin (typically some intermediate- and short-acting preparations) usually achieves rapid glucose control.24-27 Patients on oral agents (Table I) with reasonable glycemic control should have these agents continued up to the time of surgery.26,28-34 Metformin is often held 48 hours prior to surgery, but this agent may be given up to the day of surgery unless the patient has preoperative renal or hepatic disease. The glucose-lowering effects of short-acting insulin secretagogues (nateglinide, repaglinide) and the carbohydrase inhibitors are nonexistent within hours. The effects of sulfonylureas diminish rapidly (over 1-3 days) with discontinuance. The effects of metformin and the thiazolidinediones (TZDs) may last for days to a week--often through the course of the hospitalization. These durable effects of metformin and the TZDs may be important in the perioperative management of patients on oral agent therapy. Those on insulin therapy should be continued in the preoperative period. Most individuals require approximately half their total (maintenance) dose of insulin even if not allowed preoperatively to consume anything orally. This "basal" insulin can be given in the form of intermediate-acting insulins (isophane, lente, ultralente) or long-acting insulin (glargine). Supplemental short-acting insulin (subcutaneous [SC] or IV drip) may be required if there are episodes of significant hyperglycemia preoperatively. Intraoperative There are a wide variety of approaches to intraoperative glycemic control. Insulin drips are commonly used for major surgical procedures. This is usually managed by members of the anesthesia team and will not be discussed further here. Postoperative Postoperative considerations for oral glucose- lowering drugs and insulin are summarized in Table I. Patients with type 1 DM cannot have insulin withheld. Estimates of total insulin requirements are usually based on total daily preoperative requirements. As noted above, approximately one-half of all insulin is necessary for nonnutrient metabolic needs. Therefore, one-half (or more) of the preoperative dose is usually necessary in the perioperative period. Any stress that increases counterregulatory hormone levels will increase insulin needs in those with type 1 DM. Nutrient intake will also increase insulin requirements. The population with type 2 diabetes often requires insulin for adequate glycemic control in the postoperative state. This is true even if the patient had adequate glycemic control with diet or oral agents preoperatively. Furthermore, respiratory, hepatic, or renal complications following surgery may limit the use of oral agents. Insulin is safe and effective even with these complications. Many formulas have been published for insulin administration; however, insulin requirements are so variable. The best determinants to guide dosing schedules include preoperative insulin requirements with adjustments for nutrient intake, effects of stress, and associated hepatic or renal dysfunction (Table II). Insulin is the best method for glycemic control in the postoperative state for a number of reasons, including flexibility of dosing (quantity and frequency), rapid effect, and safety in the face of many comorbid conditions (renal, hepatic, cardiorespiratory). Furthermore, acceptable glucose control is usually achievable with minimal risk for hypoglycemia. Severity of hyperglycemia; preoperative insulin requirements; counterregulatory hormone responses; type, quantity, and route of nutrient administration; and renal and hepatic function determine insulin requirements. Nutrient intake is another major determinant of insulin requirements.35,36 Considerations include total caloric intake (especially carbohydrate), whether the nutrients are given parenterally or enterally, and whether the nutrient administration is continuous or in boluses. Patients who receive nutrients in the form of total parenteral nutrition (TPN) usually have insulin requirements much higher than in the preoperative state. Usual nutrient intake via TPN is associated with higher insulin requirements than for comparable caloric/carbohydrate intake via enteral formula tube feedings. For patients whose blood glucose levels are very difficult to control, the most rapid and flexible way to deliver continuous insulin is via an insulin drip. This ensures a rapid response to control hyperglycemia and low risk for hypoglycemia. Intravenous insulin administration also alleviates any variability in absorption of insulin associated with SC administration. For stable patients getting continuous feeding in the form of TPN or enteral tube feedings, fixed-dose IV insulin or frequent doses of combinations of intermediate- and short-acting insulin will provide essentially steady-state insulin concentrations. It is possible to maintain stable insulin levels with an insulin regimen with q 6-8-hour intermediate acting insulin such as isophane insulin plus q 3-4-hour administration of regular insulin (R). The fact that doses overlap leads to stable plasma insulin concentrations and stable blood glucose values as long as caloric delivery is constant. Very effective glucose control can be achieved with continuous tube feedings by using 70/30 insulin on a q 8h insulin schedule with q 4h R coverage. The total 24-hour doses of R given can then be added to the 70/30 dosage schedule the next day. Usually within 24-72 hours, stable 70/30 doses will achieve blood glucose concentrations in an acceptable range, while caloric intake via tube feedings is stable. When patients on TPN are changed to continuous tube feeding, IV access is also discontinued, necessitating a change to SC insulin. When tube feedings are stopped or decreased, insulin must be decreased simultaneously. In theory, insulin glargine would be ideal to achieve such steady-state insulin concentrations for fixed-rate nutrient intake. In reality, tube feedings are often interrupted, and this long-acting insulin would predispose patients to unacceptably high risk for hypoglycemia under this circumstance. For patients scheduled for discharge to home or an extended care facility, the tube feeding schedule may be changed to a nighttime regimen (eg, 6 pm to 6 am), but the total quantity of insulin usually stays the same (as long as caloric intake is consistent). A typical dosage regimen can be determined based on blood glucose values obtained at 6:00 am, noon, 6:00 pm, and 10:00 pm, with the insulin regimen including intermediate- or long-acting insulin given at 6:00 pm, a supplemental dose of insulin (often short-acting) at 10:00 pm, and then an intermediate- or long-acting insulin at 6:00 am. The noon blood sugar value helps determine the 6:00 am dose of insulin. The use of insulin glargine as basal insulin to replace the 6:00 am dose of intermediate-acting insulin is a reasonable consideration, but it has not yet been widely used in such patients. The above insulin regimen insures that most insulin doses are administered with minimal interruption of sleep. While few data exist on the use of parenteral and enteral nutrition from large studies performed exclusively in diabetic patients, in general, the indications for their use are considered to be the same in diabetic and nondiabetic patients.36-42 Similarly, the same beneficial effects reported for nutritional support therapy in nondiabetic patients are probably applicable to those with diabetes.

HOME HEALTH CARE Many changes occur over the first several days to weeks following discharge. For patients discharged on oral nutrient intake, there may be an associated increase in glucose levels and insulin requirements as caloric intake increases. However, a corresponding increase in physical activity and a reduction in many stress factors may decrease insulin requirements. Therefore, regular glucose self-monitoring is key to adequate glycemic control. For patients on insulin in the preoperative state, requirements often revert to preoperative levels. For persons on preoperative oral agent therapy, but discharged on insulin therapy, decisions about the nature of the pharmacotherapy are often made in the first few weeks after discharge. If preoperative glycemic control was suboptimal on two or more oral agents, continuance of therapy is generally advisable. If preoperative glycemic control was acceptable on an oral agent regimen (single or multiple medications), reversion to the oral agent regimen can be initiated. Usually, a taper of insulin is initiated simultaneously with restarting oral agents. This taper will be more rapid with agents that have a comparatively rapid onset of effects (insulin secretagogues, carbohydrase inhibitors) and slower for metformin (days to two weeks) and TZDs (weeks to months). Oral agent therapy should not be initiated if a contraindication exists to oral agent use, such as renal, hepatic, or cardiorespiratory dysfunction, after the surgery. For those in good glycemic control on diet and exercise, tapering insulin regimens may be used either with or without initiating oral agent therapy. As noted above, some patients may be discharged on enteral nutrition. If in the form of "bolus" nutritional supplements—either with meals or between meals—additional insulin may be necessary for glycemic control. A q 8h regimen of 70/30 insulin (see above) is quite effective for patients on continuous enteral feeding. For nighttime enteral feeding (eg, 6:00 pm to 6:00 am), insulin regimens need to be adjusted as noted above for the immediate postoperative period. Such regimens usually require consultation with someone experienced in insulin management in these special circumstances. The postoperative period affords an excellent opportunity to review all aspects of management of the patient with diabetes. Instruction on the importance of diet, glycemic control, and management of hypertension, dyslipidemia, and aspirin use, as well as basic guidelines for foot care should be carried out during hospitalization and following discharge.16,35,36,43-46

CONCLUSION Postoperative management of the person with DM begins in the preoperative period and extends through the hospitalization and postdischarge periods. Glycemic control during hospitalization often requires insulin therapy because of its flexibility with changing circumstances during the perioperative period. Complications of DM, including coronary disease, diminished vision, renal impairment, and neuropathy, may have significant impact on education, recovery times, and risk for adverse outcomes. The transition to glycemic control regimens after discharge is determined by several factors, including the level of glycemic control and the nature of the preoperative regimen. Therefore, treatment regimens need to be carefully individualized in patients with diabetes following the surgical procedure. References 1. Harris M. Summary. In: Diabetes in America. 2nd ed. NIH Publication 95-1468; 1995:1-13. 2. Borger MA, Rao V, Weisel RD, et al. Deep sternal wound infection: Risk factors and outcomes. Ann Thorac Surg 1998;65(4):1050-1056. 3. Pomposelli JJ, Baxter JK 3rd, Babineau TJ, et al. Early postoperative glucose control predicts nosocomial infection rate in diabetic patients. JPEN J Parenter Enteral Nutr 1998;22(2):77-81. 4. Slaughter MS, Olson MM, Lee JT Jr, Ward HB. A fifteen-year wound surveillance study after coronary artery bypass. Ann Thorac Surg 1993;56(5):1063-1068. 5. Spelman DW, Russo P, Harrington G, et al. Risk factors for surgical wound infections and bacteraemia following coronary artery bypass surgery. Australian and New Zealand Journal of Surgery 2000;70:47-51. 6. Trick WE. Scheckler WE. Tokars JI, et al. Modifiable risk factors associated with deep sternal site infection after coronary artery bypass grafting. J Thorac Cardiovasc Surg 2000;119(1):108-114. 7. Zerr KJ, Furnary AP, Grunkemeier GL, et al. Glucose control lowers the risk of wound infection in diabetics after open heart operations. Ann Thorac Surg 1997;63(2):356-361. 8. Standards of medical care for patients with diabetes mellitus. Diabetes Care 2002;25(1):213-229. 9. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993;329(14):977-986. 10. Moss SE, Klein R, Klein BE, Meuer SM. The association of glycemia and cause-specific mortality in a diabetic population. Arch Intern Med 1994;154(21):2473-2479. 11. Ohkkubo Y, Kishikawa H, Araki E, et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: A randomized prospective 6-year study. Diabetes Res Clin Pract 1995;28(2):103-117. 12. Turner R, Cull C, Holman R, for the United Kingdom Prospective Diabetes Study Group. United Kingdom Prospective Diabetes Study 17: A 9-year update of a randomized controlled trial on the effect of improved metabolic control on complications in non-insulin-dependent diabetes mellitus. Ann Intern Med 1996;124 (1 pt 2):136-145. 13. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352(9131):837-853. 14. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998;352(9131):854-865. 15. American Diabetes Association. Preventive foot care in people with diabetes. Diabetes Care 2002;25(Suppl 1):S69-S70. 16. Levin M. The diabetic foot: Pathophysiology, evaluation, and treatment. In: Levin M, O’Neal LW, eds. The Diabetic Foot. St. Louis, MO: Mosby Co;1988. 17. Gavin LA. Perioperative management of the diabetic patient. Endocrinol Metabol Clin North Am 1992;21(2):457-475. 18. Hirsch IB, McGill JB, Cryer PE, White PF. Perioperative management of surgical patients with diabetes mellitus. Anesthesiology 1991;74(2):346-359. 19. Hirsch IB, Paauw DS, Brunzell J. Inpatient management of adults with diabetes. Diabetes Care 1995;18(6):870-878. 20. Hoogwerf BJ. Perioperative management of diabetes mellitus: Striving for metabolic balance. Cleve Clin J Med 1992;59(5):447-449. 21. Hoogwerf BJ. Postoperative management of the diabetic patient. Med Clin North Am 2001;85(5):1213-1228. 22. Jacober SJ, Sowers JR. An update on perioperative management of diabetes. Arch Intern Med 1999;159(20):2405-2411. 23. Peters A, Kerner W. Perioperative management of the diabetic patient. Exp Clin Endocrinol Diabetes 1995;103(4):213-218. 24. Gillies PS, Figgitt DP, Lamb HM. Insulin glargine. Drugs 2000;59(2):253-262. 25. Puttagunta AL, Toth EL. Insulin lispro (Humalog), the first marketed insulin analogue: Indications, contraindications and need for further study CMAJ 1998;158(4):506-511. 26. Riddle MC. Overview of current therapeutic options: Session summary. Diabetes Care 1999;22(Suppl 3):C76-C78. 27. White JR Jr, Campbell RK, Hirsch I. Insulin analogues: New agents for improving glycemic control. Postgrad Med 1997;101(2):58-60,63-5,70. 28. DeFronzo, RA, Barzilai N, Simonson DC. Mechanism of metformin action in obese and lean noninsulin-dependent diabetic subjects. J Clin Endocrin Metab 1991;73(6):1294-1301. 29. DeFronzo RA, Goodman AM. Efficacy of metformin in patients with non-insulin dependent diabetes mellitus. Multicenter Metformin Study Group. N Engl J Med 1995;333(9):541-545. 30. Feinglos MN, Bethel MA. Oral agent therapy in the treatment of type 2 diabetes. Diabetes Care 1999;22(Suppl 3):C61-C64. 31. Garber AJ, Duncan TG, Goodman AM, et al. Efficacy of metformin in type II diabetes: Results of a double-blind, placebo-controlled, dose-response trial. Am J Med 1997;103(6):491-497. 32. Inzucchi SE, Maggs DG, Spollett GR, et al. Efficacy and metabolic effects of metformin and troglitazone in type II diabetes mellitus. N Engl J Med 1998;338(13):867-872. 33. Lebovitz HE. Effects of oral antihyperglycemic agents in modifying macrovascular risk factors in type 2 diabetes. Diabetes Care 1999;22( Suppl 3):C41-C44. 34. Saltiel AR, Olefsky JM. Thiazolidinediones in the treatment of insulin resistance and type II diabetes. Diabetes 1996;45(12):1661-1669. 35. Evidence-based nutrition principles and recommendations for treatment and prevention of diabetes and related complications. Diabetes Care 2002;25(1):202-212. 36. American Diabetes Association. Translation of diabetes nutrition recommendations for health care insitutions. Diabetes Care 2002;25(1)(Suppl 1):S61-S63. 37. Beale RJ, Brug DJ, Bihari DJ. Immunonutrition in the critically ill: A systematic review of clinical outcome. Crit Care Med 1999;27(12):2799-2805. 38. Coulston AM. Enteral nutrition in the patient with diabetes mellitus. Curr Opin Clin Nutr Metab Care 2000;3(1):11-15. 39. The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med 1997;157(21):2413-2446. 40. Matarese LE. Enteral feeding solutions. Gastrointest Endosc Clin N Am 1998;8(3):593-609. 41. Pitts DM, Kilo KA, Pontious SL. Nutritional support for the patient with diabetes. Crit Care Nurs Clin North Am 1993;5(1):47-56. 42. Wright J. Total parenteral nutrition and enteral nutrition in diabetes. Curr Opin Clin Nutr Metab Care 2000;3(1):5-10. 43. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285(19):2486-2497. 44. American Diabetes Association. Aspirin Therapy in Diabetes. Diabetes Care 2002;25(Suppl 1):S78-S79. 45. Franz MJ, Bantle JP, Beebe CA, et al. Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care 2002;25(1):148-198. 46. Friedrich CA, Rader DJ. Management of lipid disorders. Rheum Dis Clin North Am 1999;25(3):507-520.1.

Annals of Long-Term Care - ISSN: 1524-7929 - Volume 11 - Issue 12 - December 2003

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