Transitional Feeding and Discontinuing PN 44,45

PARENTERAL NUTRITION (PN) - ADULT

CENTRAL 3-in-1 Dextrose _____ g

VII. Transitional Feeding and Discontinuing PN 44,45

A. The ultimate goal for patients receiving PN is to return to as nearly normal food intake as tolerated. The period during which oral or enteral feeding is initiated and PN is discontinued may be termed the transitional period. The transition from PN to oral intake or enteral tube feeding should be accomplished in an orderly fashion to avoid the potential for deterioration in nutritional status when PN is discontinued.

1. In pediatric patients, discontinuation of PN is generally a more gradual process than in adult patients.

a) PN is tapered as enteral feeds are advanced. Ideally, the com- bination of PN and enteral feedings will meet all estimated nutritional goals during the transitional period.

b) In practice, PN is generally continued until about 75% to 80% of energy needs (90–100 kcal/kg) are met enterally.

2. For many adult patients, PN may be discontinued as soon as they are able to tolerate solid foods. These patients are usually younger, well nourished before PN, not debilitated, free of malignancy, and without oral intake for less than 1 to 2 weeks.

3. For other adult patients, a detailed transitional feeding plan may be needed. Candidates for transitional feeding include those

who are elderly or debilitated, those with malignancy, and those who eat ethnic foods not available in the hospital setting.

4. Adult patients with known diabetes mellitus or clinically induced insulin resistance require special monitoring to set up a safe transitional feeding plan.

B. To guide the transition from PN to full oral intake, a bedside calo- rie count may be performed when the patient is eating a substantial amount of food with a consistent appetite or effort but unsure of how much may have been tolerated or consumed. This count may be used to guide the reduction or discontinuation of PN.

C. Although it has been documented that nondiabetic adult patients suffer minimal ill effects, abrupt discontinuance of PN may poten- tiate rebound hypoglycemia in patients who are not being fed orally or enterally.

1. PN may be rapidly discontinued in an adult patient who is toler- ating tube feeding in amounts adequate to maintain serum glucose levels.

2. Decreasing the PN infusion rate by one-half for 1 to 2 hours before discontinuation may minimize the risk of rebound hypoglycemia.

3. If PN is abruptly discontinued, a 10% dextrose solution may be administered for a few hours. This practice is unnecessary when discontinuing PPN.

4. Capillary glucose concentrations may be measured 30 to 60 minutes after cessation of a central PN formulation, and oral or IV carbohydrate can be given as appropriate if hypoglycemia is suspected.

D. Oral or enteral tube feeding may be initiated when the patient has demonstrated return of GI function.

E. Initiation of oral intake requires GI function, minimal risk for aspiration, and patient motivation.

F. In some circumstances, a swallowing evaluation may be useful in determining readiness for oral feeding and can dictate the type and texture of foods introduced.

G. PN may have a negative effect on appetite. If more than 25% of caloric needs are provided as PN, reduced oral intake can be expected.⁴⁶

1. When oral intake equals 500 kcal/day in an adult patient, the carbohydrate and protein in the PN should be reduced by an amount equal to the amount consumed orally.

2. Subsequent decreases in the PN should continue as oral intake increases.

3. Once an adult patient is taking 60% of goal energy and protein via the oral route, PN may be stopped.

H. For adults who do not achieve acceptable oral intake within a few days, enteral tube feeding should be considered.

I. For adults who have been receiving substantial amounts of elec- trolytes in the PN, oral or IV electrolyte supplements may be needed.

(Parenteral Nutrition Management chapters from the 1st edition were contributed by Annalynn Skipper, Keith Millikan, Kristy Gibbons, Nancy Cyr, Michael L. Christensen, and Richard A. Helms)

R E F E R E N C E S

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Washington, DC: National Academy Press; 1989:174–194.

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3. Baumgartner TG. Clinical Guide to Parenteral Micronutrition.3rd ed.

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7. McMahon M, Manji N, Driscoll DF, Bistrian BR. Parenteral nutrition in patients with diabetes mellitus: theoretical and practical considerations.

J Parenter Enteral Nutr.1989;13:545–553.

8. Kalhan SC, Kilic I. Carbohydrate as nutrient in the infant and child: range of acceptable intake. Euro J Clin Nutr.1999;53(suppl 1):S94–S100.

9. Intravenous Nurses Society. Infusion nursing: standards of practice.

J Intravenous Nurs.2000;23(suppl):S1–S88.

10. A.S.P.E.N. Board of Directors and the Task Force on Standards for Spe- cialized Nutrition Support for Hospitalized Adult Patients. Standards for specialized nutrition support: adult hospitalized patients. Nutr Clin Pract.

2002;17:384–391.

11. Harden JL, Kemp C, Mirtallo J. Femoral catheters increase risk of infection in total parenteral nutrition patients. Nutr Clin Pract.1995;10:60–66.

12. Centers for Disease Control and Prevention. Guidelines for the prevention of intravascular catheter-related infections. MMWR.2002;51(No. RR-10).

13. Bethune K, Allwood M, Grainger C, Wormleighton C. British Pharmaceu- tical Nutrition Group Working Party. Use of filters during the preparation and administration of parenteral nutrition: position paper and guidelines prepared by a British pharmaceutical nutrition group working party. Nutri- tion.2001;17:403–408.

14. Task Force for Safe Practices for Parenteral Nutrition. Safe practices for parenteral nutrition. J Parenter Enteral Nutr.2004;28:S39–S70.

15. Food and Drug Administration. Safety alert: hazards of precipitation associated with parenteral nutrition. Am J Hosp Pharm.1994;51:1427–1428.

16. Dickerson RN. Di(2-ethylhexyl)phthalate as a plasticizer for intravenous bags and tubing: a toxicological quandary.Nutrition.1997;13:1010–1012.

17. Krzywda EA, Andris DA, Edmiston CE, Wallace JR. Parenteral access devices. In: Gottschlich MM, ed. The Science and Practice of Nutrition Support: A Case-Based Core Curriculum.Dubuque, IA: Kendall/Hunt;

2001:225–250.

18. JCAHO. 2005 National Patient Safety Goals FAQs. www.jcaho.org/

accredited+organizations/patient+safety/05+npsg/05_npsg.html Accessed December 8, 2004

19. US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupa- tional Safety and Health Settings (NIOSH). Preventing Needlestick Injuries in Health Settings.NIOSH Publication No 2000-108. Cincinnati, OH:NIOSH;November; 1999.

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Enforcement Procedures for the Occupational Exposure to Bloodborne Pathogens. Directives No CPL 2-2.44D.Effective date: November 5, 1999.

US Department of Labor, Washington DC, 1999.

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Occupational Exposure to Bloodborne Pathogens; Needlesticks and Other Sharp Injuries; Final Rule Federal Legislation, Public Law 106-430.Effec- tive date: April 18, 2001. US Department of Labor, Washington DC, 2001.

22. A.S.P.E.N. Board of Directors. Clinical Pathways and Algorithms for Delivery of Parenteral and Enteral Nutrition in Adults.Silver Spring, MD:

American Society for Parenteral and Enteral Nutrition; 1998.

23. Nehme AE. Nutritional support of the hospitalized patient: the team con- cept. JAMA.1980;243:1906–1908.

24. Kerr TM, Lutter KS, Moeller DM, et al. Upper extremity venous thrombosis diagnosed by duplex scanning. Am J Surg.1990;160:202–206.

25. Horattas MC, Wright DJ, Fenton AH, et al. Changing concepts of deep venous thrombosis of the upper extremity: report of a series and review of the literature. Surgery.1988;104:561–567.

26. Shulman RJ, Reed T, Pitre D, et al. The use of hydrochloric acid to clear obstructed central venous catheters. J Parenter Enteral Nutr.1988;12:

509–510.

27. Pennington CR, Pithie AD. Ethanol lock in the management of catheter occlusion. J Parenter Enteral Nutr.1987;11:507–508.

28. Borg FT, Timmer J, de Kam SS, Sauerwein HP. Use of sodium hydroxide solution to clear partially occluded vascular access ports. J Parenter Enteral Nutr.1993;17:289–291.

29. Andris DA, Krzywda EA. Catheter pinch-off syndrome: recognition and management. J Intravenous Nurs.1997;20:233–237.

30. Maki DG, Stolz SM, Wheeler S, et al. Prevention of central venous catheter–related bloodstream infection by use of an antiseptic-impregnated catheter: a randomized, controlled trial. Ann Intern Med.1997;127:

257–266.

31. Adal KA, Farr BM. Central venous catheter-related infections: a review.

Nutrition.1996;12:208–213.

32. Fleming CR. Hepatobiliary complications in adults receiving nutrition support. Dig Dis.1994;12:191–198.

33. Suita S, Ikeda K, Nagasaki A, et al. Follow-up studies of children treated with a long-term intravenous nutrition during the neonatal period. J Pediatr Surg.1982;17:37–42.

34. Pelegano JF, Rowe JC, Carey DE, et al. Simultaneous infusion of calcium and phosphorus in parenteral nutrition for premature infants: use of physi- ologic calcium/phosphorus ratio. J Pediatr.1989;114:115–119.

35. Brooks MJ, Melnik G. The refeeding syndrome: an approach to under- standing its complications and preventing its occurrence. Pharmacother- apy.1995;15:713–726.

36. Collins JW Jr, Hoppe M, Brown K, et al. A controlled trial of insulin infusion and parenteral nutrition in extremely low birth weight infants with glucose intolerance. J Pediatr.1991;118:921–927.

37. McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia.

Crit Care Clin.2001;17:107–124.

38. McCowen KC, Bistrian BR. Hyperglycemia and nutrition support: theory and practice. Nutr Clin Pract.204;19:235–244.

39. Marcuard SP, Dunham B, Hobbs A, Caro JF. Availability of insulin from total parenteral nutrition solutions. J Parenter Enteral Nutr.1990;14:262–264.

40. Farrag HM, Cowett RM. Glucose homeostasis in the micropremie. Clin Perinatol.2000;27:1–22.

41. Werlin SL, Wyatt D, Camitta B. Effect of abrupt discontinuation of high glucose infusion rates during parenteral nutrition. J Pediatr.1994;124:

441–444.

42. Sacks GS, Mouser JF. Is IV lipid emulsion safe in adult patients with hypertriglyceridemia? Nutr Clin Pract.1997;3:120–123.

43. Brown RO, Dickerson RN. Drug-nutrient interactions. Am J Managed Care.1999;5:345–352.

44. Wagman LP, Miller KB, Thomas RB, Newsome HH, Weir GC. The effect of acute discontinuation of total parenteral nutrition. Ann Surg.1986;204:

524–529.

45. Winkler MF, Pomp A, Caldwell MD, Albina JE. Transitional feeding: the relationship between nutritional intake and plasma protein concentrations.

J Am Diet Assoc.1989;89:969–970.

46. Gil KM, Skeie B, Kvetan V, Askanazi J, Freidman MI. Parenteral nutrition and oral intake: effect of glucose and fat infusions. J Parenter Enteral Nutr.

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S U G G E S T E D R E A D I N G S

Klein S, Kinney J, Jeejeebhoy K, et al. Nutrition support in clinical practice:

review of published data and recommendations for future research direc- tions. J Parenter Enteral Nutr.1997;21:133–156.

Rombeau JL, Rolandelli RR, eds. Clinical Nutrition: Parenteral Nutrition.

3rd ed. Philadelphia, PA: WB Saunders; 2001.

Michael S. Nyffeler, PharmD, BCNSP;

Eric Frankel, PharmD, BCNSP; Edmund Hayes, PharmD;

Stephanie Mighdoll, PharmD

9

Drug-Nutrient Interactions

Introduction

The goal of a multidisciplinary approach to monitoring enterally and parenterally fed patients for drug-nutrient interactions is to maximize the therapeutic response to the medication administered without adversely affecting enteral nutrition tolerance. This chapter addresses principles of drug absorption, distribution, and metabolism along with potential drug-nutrient interactions in these patients.

I. Background

II. Enteral Incompatibilities

III. Medication Administration via Enteral Feeding Tubes IV. Parenteral Considerations

V. Effects of Medications on Clinical Laboratory Values VI. Effects of Drugs on Nutrition and Metabolism References

I. Background

A. Absorption 1. Enteral

a) Absorption requires movement of medication from the gas- trointestinal (GI) tract into the general circulation. Not all of a drug dose is necessarily absorbed, and not all absorbed drug reaches the systemic circulation as active drug. Some of the absorbed drug is eliminated or metabolized in the GI tract or liver before it reaches its site of action. Absorption of medication is generally what is affected when drug-nutrient interactions occur in enterally fed patients.

b) Bioavailability is the percentage of the original dose that reaches the systemic circulation as active drug¹; the process of bioavailability is distinctly different from absorption.

c) Disintegration and dissolution of a drug in the aqueous diges- tive fluid must occur prior to absorption, if the medication is not already in solution. Medications that are formulated as sus- pensions must also undergo dissolution. Once a medication has dissolved, it can then diffuse across the intestinal mucosa.² (1) For most solid-dose forms (tablets, capsules), the rate-

limiting step of absorption is dissolution.²Disintegration is the process of a solid-dose form breaking down into smaller particles, which improves the rate at which a drug then dissolves so that absorption may occur. Stomach churning in the presence of aqueous fluids aids in disintegration and dissolution. Once the components of the tablet have been adequately reduced in size, they leave the stomach and enter the small bowel, where the majority of absorption occurs. The small bowel provides a large surface area and is well perfused to enhance the absorption process.²

(2) For liquid medications in solution, the rate-limiting step to absorption is blood perfusion of the intestines, where absorption takes place.²Adequate perfusion of the small bowel is necessary for proper absorption. Disease states, edema, surgery, and sepsis may decrease perfusion.

(3) Absorption of medication may be altered by factors such as the presence of other drugs, the gastric emptying rate, the route of administration, the location of the distal tip of the enteral tube, or the presence of food.

d) Factors that alter medication absorption (1) Approaches to enhance absorption

(a) Use liquid medications to bypass the dissolution step; if tablets are used, they should be pulverized to enhance dissolution and subsequent absorption.³

(b) Administer liquid medications or pulverized tablets with adequate fluid. Fluid helps expand the stomach, thereby enhancing the rate of gastric emptying.

(c) Many enterally fed patients do not meet their daily fluid requirements with enteral feeding alone, and they require additional free water throughout the day. When- ever possible, administer additional free water flushes in conjunction with scheduled medications. These flushes provide an excellent medium for delivery of medication, enhance its absorption, and maintain enteral tube patency.

(2) Factors that may inhibit optimal absorption

(a) Enteral tubes are placed with the distal tip in the stomach, duodenum, or jejunum. Absorption may become an issue for medications when the distal end of the enteral feeding tube is placed beyond the main site of absorption.

i) Itraconazole is a medication that requires an acidic environment to ensure proper dissolution when administered as a solid dosage form. Absorption will be poor if delivered in the jejunum because dissolution is inadequate. The liquid form, on the other hand, is already dissolved and does not require the acidic environment of the stomach for dissolution to occur; therefore, it is amenable to postpyloric administration. Extemporaneous preparations of itraconazole are not reliably absorbed.^4–5No studies to date have evaluated itraconazole absorption with concurrent enteral feedings.

ii) The main site of absorption of ciprofloxacin is the upper part of the intestinal tract.⁶Studies have indi- cated mixed results with respect to ciprofloxacin absorption via feeding tubes. When ciprofloxacin is administered via a jejunostomy tube, reduction in

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

absorption may result in treatment failure; therefore, this type of administration is not advised.⁷ (b) Medications delivered directly into the jejunum rather

than the stomach can be expected to have a decreased transit time, reducing the amount of time during which the medication can be absorbed. Tablets delivered directly into the jejunum lose the positive churning and dissolution activity of the stomach, yet the jejunum is still a viable option for administration of most medications.³

(c) Some medications (eg, penicillin, tetracycline, rifampin), are better absorbed when taken “on an empty stomach.” Patients who receive continuous feeding by gastric tube never have an empty stomach.

To optimize absorption of such medications, tube feeding should be held approximately 30 to 60 minutes before and 30 minutes after the medication is administered; the tube-feeding schedule should then be readjusted to meet the patient’s total 24-hour nutritional needs.

(d) If patients develop GI intolerances during tube feedings (eg, nausea, vomiting, diarrhea, increased gastric resid- uals, cramping), the medication profile should be reviewed for potential causative agents. Whenever possible, change to medications with therapeutic equiva- lents or change the route of administration before considering discontinuation of tube feeding.

(e) Use of prokinetic agents (eg, metoclopramide) may decrease transit time, alter absorption of some medications, and contribute to diarrhea.⁸

(f) Medications that delay gastric emptying or decrease GI motility

i) Anticholinergics (eg, antihistamines, tricyclic antidepressants, phenothiazines, medications for Parkinson’s disease) cause smooth muscle relax- ation and inhibit gastric motility.⁹

ii) Aluminum-containing antacids delay gastric emptying.

iii) Narcotics interfere with normal peristalsis and delay gastric emptying.⁹

2. Parenteral

a) Parenteral routes of drug delivery. Technically, the term parenteral refers to all drug administration other than by the GI tract. Commonly, the term is used to refer to the intravenous (IV) route, where the drug is injected into the body. Par- enteral delivery of medication avoids the issue of absorption, as the entire dose will enter the body. Once the drug is in the bloodstream, the action of the drug is the same without regard for administration route. With few exceptions, oral administration of drugs is favored, as is oral administration of nutrients.

b) Effect of route on kinetics. A large variety of drug delivery routes fall under the umbrella of parenteral administration.

Rapid IV infusion (IV push), controlled IV infusion over a short period of time (IV piggyback or secondary administration), and continuous IV infusion (IV drip) are all common parenteral drug administration methods. Intra-arterial delivery is also done for certain drugs to deliver a concentrated dose to a specific organ.

c) Effect of entry point into bloodstream (first-pass effect or lack of same affecting systemic dose). The point at which a drug

enters the bloodstream can affect its bioavailability. Most parenterally administered drugs enter the bloodstream via the capillary or venous circulation. In contrast, enterally administered drugs (with a few exceptions for gastric, sublingual, and buccal administration) will enter the portal circulation and be transported to the liver before entering the general circulation.

Since this occurs only after initial absorption, it is referred to as the first-pass effect. The liver is the major site of biotransformation of organic substances and exerts a profound effect on many enterally absorbed substances. Dosage differences for drugs given orally versus parenterally can be large; in the case of propranolol, for instance, the oral dose is approximately 10 times the IV dose. First-pass effect can also change the action of a drug. The composition of early pediatric parenteral amino acids was based on the amino acids in human breast milk. However, because human breast milk undergoes biotransformation by the liver before entering the general circulation and parenteral amino acids bypass the liver entirely, parenteral amino acids for neonates are now designed to match the serum aminograms of breast-fed infants, not the amino acid composition of human breast milk.

B. Distribution

1. Volume of distribution defined. When a substance enters the body, it is distributed via the bloodstream to many tissues. It achieves varying concentrations in these tissues based on the solubility of the drug and its affinity for each tissue. If a drug has a high affinity for muscle or fat, serum levels of the drug will be lowered. An artificial construct called apparent volume of distribution or simply volume of distribution (Vd) is used to predict the kinetics of a substance. Volume of distribution is defined as the volume in which the substance entering the body would need to be diluted to achieve the observed serum levels. The volume of distribution is expressed in liters per kilogram of body weight to correct for differing body weights. If the drug is highly water soluble and primarily found in body water, it will have a volume of distribution of 0.6 L/kg. The same dose of a drug that is lipid soluble will achieve lower serum levels, and its volume of distribution will be greater than 0.6 L/kg. For example, digoxin is widely distributed in body tissue and has a Vdof 7 L/kg. A drug that is concentrated intravascularly will have a Vdless than 0.6 L/kg.

Sulfisoxazole has a Vdof 0.16 L/kg.¹⁰

2. Protein binding. Many substances bind to protein. Protein binding may increase the length of time a drug remains in the body while also attenuating its serum levels. The metabolism of the substance by the liver may be decreased, as only the unbound substance is available for biotransformation.

3. Solubility and tissue distribution. The solubility of a substance has a profound effect on its distribution within the body. Water- soluble or hydrophilic substances are principally distributed within the fluid compartments of the body.

C. Metabolism.

1. Liver enzyme systems. Many drugs are metabolized via the cyto- chrome P-450 (CYP450) enzyme system. Although numerous enzyme families within CYP450 have been identified, CYP3A4 is involved with the metabolism of most drugs currently on the mar- ket.¹¹Other isoenzymes commonly associated with drug metabolism include CYP1A2, CYP2C19, and CYP2D6.¹²Nutrients, like drugs, can inhibit or induce the effects of these metabolic enzymes. When the enzyme that is responsible for the metabolism of a particular drug is induced, the serum level of the drug is decreased. The opposite effect on the drug would occur if the

Dalam dokumen The A.S.P.E.N. Nutrition Support Practice Manual, 2nd Edition (Halaman 136-140)