Parenteral Feeding in Diabetes Patients — RDs Can Play a Pivotal Role in Glycemic Control

December 2011 Issue

Parenteral Feeding in Diabetes Patients — RDs Can Play a Pivotal Role in Glycemic Control
By Sandra I. Austhof, MS, RD, LD, CNSD, and Monica A. Habib, MS, RD, LD, CNSC
Today’s Dietitian
Vol. 13 No. 12 P. 44

A hospitalized patient with diabetes mellitus has been receiving parenteral nutrition (PN) for a couple of weeks. Due to the medications he takes for a variety of illnesses, he often experiences sudden spikes in blood glucose. To gain glycemic control, the medical and nutrition team closely monitors his blood sugar levels and makes careful adjustments to his medications to avoid complications that can worsen his condition.

Such a scenario is all too common in diabetes patients receiving PN and who face the unique challenges of maintaining glycemic control for the long haul. Hyperglycemia is the most common metabolic complication of PN and can be caused by overfeeding, metabolic stress, infection, chromium deficiency, or the use of steroids and octreotide (a somatostatin analog used to curtail gastrointestinal [GI] losses). Infusions of IV dextrose can worsen glucose control, which can increase the demand on already dysfunctional pancreatic islet cells. Patients with type 1 and type 2 diabetes often require greater amounts of insulin from baseline during a PN infusion to lower blood sugar.1-3 The presence of poor glucose control alters immune function, increases the inflammatory response, and can lead to endothelial dysfunction and cardiovascular complications.4-7

Given the dire consequences of poor glycemic control in these patients, it’s imperative for RDs to understand the complexities of diabetes and PN management. This article will review the indications for PN, the importance of glycemic control, and the complications associated with PN and will provide strategies for RDs to help stabilize blood glucose levels and improve patient outcomes.

When is PN Necessary?
Indications for PN are the same for diabetes patients as they are for those without the disease. PN is used when the GI tract is nonfunctional.8 For example, PN is required when patients develop high-output enterocutaneous fistula, short-bowel syndrome, severe malabsorption, a small-bowel obstruction, paralytic ileus, intestinal or mesenteric ischemia, radiation enteritis, graft-vs.-host disease, severe colitis, chylothorax, a small-bowel leak, or intractable vomiting or diarrhea.

PN is also administered when the GI tract becomes inaccessible or is unsafe to use when a patient experiences GI bleed or hemodynamic instability (requiring escalating doses of vasopressors) or when nutritional needs can’t be met enterally.8 However, if at all possible, the use of enteral nutrition in patients who have diabetic gastroparesis is recommended due to the risk of thrombosis and infection associated with PN.9

Benefits of Blood Glucose Control
Diabetes patients whose blood sugar is controlled experience many benefits from PN, ranging from fluid maintenance to improved immune function. Several studies show that euglycemia improves morbidity and mortality in medical and surgical ICU patients.10,11 A study by van den Bergh and colleagues12 illustrated that glycemic control reduced mortality, critical illness, polyneuropathy, bacteremia, and inflammation. Controlled blood sugar also has been shown to improve fluid balance by maintaining the filtered glucose load inside the tubular lumen of the kidney, therefore decreasing the risk of osmotic diuresis and urinary loss of electrolytes and water.10 For noncritically ill patients, a safe glucose range of 100 to 150 mg/dL is recommended.13 Stricter glycemic control in critically ill patients, ranging from 80 to 110 mg/dL12, has been advised; however, the risk for hypoglycemia (plasma glucose less than 70 mg/dL) becomes a concern.

Hypoglycemic Complications
Hypoglycemia is more prevalent in type 1 diabetes and can cause anxiety, heart palpitations, sweating, tremors, and paresthesias.14 Patients also can suffer from neurological symptoms such as changes in behavior, cognitive dysfunction, seizures, or coma. Patients with a long history of diabetes may have hypoglycemic unawareness due to reduced sympathoadrenal responses.10,14 Treatment for hypoglycemia in PN patients includes administration of the following:

• 1/2 cup fruit juice or regular soda or 1 cup low-fat milk if the patient is conscious and able to swallow;

• 15 g of 40% dextrose oral gel inside the cheek in a patient who’s semiconscious;

• a 25-mL syringe of dextrose 50% in water; or

• a 1-mg subcutaneous injection of glucagon if the patient is unconscious or unable to swallow or take anything by mouth, or if the patient has no IV access.

A nurse should recheck blood glucose levels 15 minutes after administering one of these treatments. If the patient’s blood sugar level remains below 70 mg/dL, the nurse will give the patient one of the treatments again for a maximum of three times, and the physician may consider temporarily stopping the PN.

Adverse Effects of Hyperglycemia
As mentioned, the most common metabolic complication in patients with and without diabetes mellitus is hyperglycemia. High blood glucose levels negatively affect both the micro- and macrovascular cardiovascular system, including endothelial cell dysfunction. It triggers neuronal damage, causing brain ischemia, and may produce oxidative stress leading to cell injury.11 Hyperglycemia also can cause electrolyte disturbances such as hypernatremia, hyponatremia, hypokalemia, and hypophosphatemia. Hypernatremia and hyponatremia are determined by the balance between the dilution of sodium due to osmotic water movement out of the cells and the concentration of sodium due to water loss in excess of sodium.15 Hypokalemia and hypophosphatemia can occur as a result of the extracellular shift of potassium and phosphorus due to osmotic diuresis. In addition, hypokalemia may be caused by increased GI losses, glycogenolysis, or proteolysis.15

Medication Contraindications
Issues can arise as a result of the medications a patient receives intravenously with PN because few drugs are compatible with PN. Generally, adding medications isn’t recommended because of the potential drug-nutrient interactions, the inability to adjust the dose, or the need to discontinue the drug without having to discontinue PN. However, sometimes it’s necessary to add medications to the PN bag, such as regular insulin, to control elevated blood sugar.

Regular insulin, octreotide, corticosteroids, and H2 blockers are a few of the medications physicians can add to PN. Octreotide is a medication used to decrease GI secretions and slow GI motility in patients with increased GI losses from an ostomy or diarrhea. However, octreotide can raise blood glucose and, less frequently, lower blood sugar levels. Corticosteroids, used to reduce inflammation, also can elevate glucose levels. Therefore, the nutrition and medical team need to monitor blood sugar carefully when giving patients these medications. When these drugs are tapered or discontinued, RDs must make adjustments to the PN insulin with the physician’s approval.

PN Management Strategies
Due to these complexities, managing PN involves daily monitoring of plasma glucose, electrolytes, and fluid balance. RDs should initiate PN when plasma glucose levels are under control (less than 180 mg/dL).16

When beginning PN, dietitians should restrict the number of carbohydrates given to 100 to 150 g.16 Research has suggested limiting dextrose administration to 1.5 to 2 mg/kg of body weight per minute.17 RDs should ensure that standard, regular insulin and hypoglycemia orders are in place and signed by the physician as a safety net before initiating PN (see table below) to manage possible severe blood sugar highs and lows, which are detrimental to patients. A nurse should monitor capillary blood glucose levels every six hours until they’re consistently less than 150 mg/dL.

Since regular insulin is compatible with PN formula, a nurse will add it as needed. Nurses can determine the initial dose by using 0.1 units of regular insulin per gram of dextrose given.13 They can base the amount of insulin given in subsequent bags on two-thirds of the total amount of insulin administered the previous day.1,11 For example, if a nurse gave a patient 16 units of sliding-scale insulin on day 1, the nurse would add 10 units (two-thirds of 16 units) to PN on day 2. If hyperglycemia continues after exceeding 0.3 units of regular insulin per gram of dextrose, a nurse would consider adding a separate IV insulin infusion.16 However, an IV bolus of insulin shouldn’t be given, as severe hypokalemia may quickly develop because it’s short acting. Long-acting insulin, such as glargine, administered subcutaneously as a basal dose, has been shown to improve glycemic control in diabetes patients receiving PN.18

Dietitians can advance dextrose calories only after glucose levels are well controlled. If the PN contains insulin, it’s important to maintain the ratio of PN insulin to dextrose when increasing or decreasing dextrose calories. If hyperglycemia persists despite daily increases in insulin, RDs can lower dextrose calories and replace them with fat calories (using a three-in-one formulation). However, recent studies have demonstrated that the infusion of fat emulsion increases free fatty acids, leading to insulin resistance and impaired glucose tolerance.19,20 In addition, RDs should stop PN when serum glucose becomes greater than 400 mg/dL and replace it with IV normal saline infusion started at the same rate. Once glucose is controlled, RDs can start a new PN bag with adjusted insulin. Also, additional chromium should be included in the PN if a deficiency is present since chromium regulates insulin action.

Team Approach
Nutrition professionals face several challenges when trying to gain glycemic control in adult hospitalized patients with diabetes mellitus who require PN. Hyperglycemia is a risk factor for morbidity and mortality and is a common complication. However, careful monitoring of blood glucose, electrolytes, and fluid balance is imperative for optimal patient outcomes, which can be achieved with the help of a multidisciplinary team approach of dietitians, nurses, pharmacists, and physicians.

— Sandra I. Austhof, MS, RD, LD, CNSD, is a nutrition support dietitian at the Cleveland Clinic and has worked in the field for more than 30 years.

— Monica A. Habib, MS, RD, LD, CNSC, is a nutrition support dietitian at the Cleveland Clinic and recently graduated with a master’s degree in nutrition from Kent State University.

Table 1

Guidelines for Subcutaneous Regular Insulin Administration
Glucose (mg/dL)	Dose of Regular Insulin (units)
151-200	2-4
201-250	4-8
251-300	6-12
301-350	8-16
351-400	10-20

— Source: Cleveland Clinic

References
1. Overett TK, Bistrian BR, Lowry SF, Hopkins BS, Miller D, Blackburn GL. Total parenteral nutrition in patients with insulin-requiring diabetes mellitus. J Am Coll Nutr. 1986;5(1):79-89.

2. Park RH, Hansell DT, Davidson LE, Henderson G, Legge V, Gray GR. Management of diabetic patients requiring nutritional support. Nutrition. 1992;8(5):316-320.

3. Hongsermeier T, Bistrian BR. Evaluation of a practical technique for determining insulin requirements in diabetic patients receiving total parenteral nutrition. JPEN J Parenter Enteral Nutr. 1993;17(1):16-19.

4. 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(3):978-982.

5. Cheung NW, Napier B, Zaccaria C, Fletcher JP. Hyperglycemia is associated with adverse outcomes in patients receiving total parenteral nutrition. Diabetes Care. 2005;28(10):2367-2371.

6. Lin LY, Lin HC, Lee PC, Ma WY, Lin HD. Hyperglycemia correlates with outcomes in patients receiving total parenteral nutrition. Am J Med Sci. 2007;333(5):261-265.

7. Pasquel FJ, Spiegelman R, McCauley M, et al. Hyperglycemia during total parenteral nutrition. Diabetes Care. 2010;33(4):739-741.

8. Saalwachter AR, Evans HL, Willcutts KF, et al. A nutrition support team led by general surgeons decreases inappropriate use of total parenteral nutrition on a surgical service. Am Surg. 2004;70(12):1107-1111.

9. Jones MP. Management of diabetic gastroparesis. Nutr Clin Pract. 2004;19(2):145-153.

10. McDonnell ME, Apovian CM. Diabetes mellitus. In: Gottschlich MM (ed). The A.S.P.E.N Nutrition Support Core Curriculum: A Case-Based Approach—The Adult Patient. Silver Spring, Md.: American Society for Parenteral and Enteral Nutrition; 2007:676-694.

11. Clement S, Braithwaite SS, Magee MF, et al. Management of diabetes and hyperglycemia in hospitals. Diabetes Care. 2004;27(2):553-591.

12. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001;345(19):1359-1367.

13. McMahon MM. Management of parenteral nutrition in acutely ill patients with hyperglycemia. Nutr Clin Pract. 2004;19(2):120-128.

14. Cryer PE, Davis SN, Shamoon H. Hypoglycemia in diabetes. Diabetes Care. 2003;26(6):1902-1912.

15. Kitabchi AE, Rose BD. Clinical features and diagnosis of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults. Available at: http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults?source=see_link&anchor=H2 - H18. Accessed October 3, 2011.

16. Sacks G, Mayhew S, Johnson D. Parenteral nutrition implementation and management. In: Merritt R (ed). The A.S.P.E.N. Nutrition Support Practice Manual. 2nd ed. Silver Spring, Md.: American Society for Parenteral and Enteral Nutrition; 2005:108-117.

17. Via M, Mechanick JI. Inpatient enteral and parenteral nutrition for patients with diabetes. Curr Diab Rep. 2011;11(2):99-105.

18. Fatati G, Mirri E, Del Tosto S, et al. Use of insulin glargine in patients with hyperglycaemia receiving artificial nutrition. Acta Diabetol. 2005;42(4):182-186.

19. Umpierrez GE, Smiley D, Robalino G, et al. Intravenous intralipid-induced blood pressure elevation and endothelial dysfunction in obese African-Americans with type 2 diabetes. J Clin Endocrinol Metab. 2009;94(2):609-614.

20. Liu Z, Liu J, Jahn LA, Fowler DE, Barrett EJ. Infusing lipid raises plasma free fatty acids and induces insulin resistance in muscle microvasculature. J Clin Endocrinol Metab. 2009;94(9):3543-3549.