TRIPASS XR تري باس

 

79–81 The patient can experience symptoms of reflux similar to a Zollinger–

Ellison syndrome with epigastric pain and burning. Medications that decrease GI

tract motility (antidiarrheals) and secretions (H2 blockers and proton pump

inhibitors) are frequently necessary to reduce the volume of gastric secretions and

minimize the damaging effects of hypersecretion of gastric acid. These agents are

also important in the management of fluid and electrolyte imbalances because of

excessive GI fluid losses. Patients with extensive small bowel resection and an intact

colon, such as D.D., may experience diarrhea as a result of bile salt depletion.

1,73,74

Octreotide may help in decreasing diarrhea in patients with SBS. Octreotide

reduces a variety of GI secretions and slows jejunal transit, but the effects are often

short-lasting and have not shown improved nutrient absorption.

82

It is important to be

mindful that most oral medications are absorbed within the first 50 cm of the jejunum.

Delayed-release medications should be avoided.

Patients with SBS are at risk for having vitamin and mineral deficiencies,

especially folate, vitamin B12

, vitamin D, selenium, and zinc. These patients should

receive supplemental vitamin B12 and IV parenteral or oral liquid multivitamin

supplements. GI losses of trace minerals, particularly zinc and selenium, are

increased in SBS, and these minerals should be supplemented.

73,74

D.D. should be continued on PN support and will most likely need PN therapy at

home to sustain his nutrient and fluid requirements. Since oral ranitidine in not an

option, the treatment team

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orders ranitidine 150 mg to be added to D.D.’s PN formula to manage

hypersecretion of gastric fluids and diarrhea. D.D.’s fluid status must be monitored

and evaluated daily for clinical signs of dehydration or fluid overload. Electrolyte

abnormalities, including hyponatremia, hypokalemia, hypomagnesemia,

hypocalcemia, and metabolic acidosis, should be anticipated.

74

CASE 38-4, QUESTION 4: On hospital day 10, he presents with a fever and green, purulent fluid draining

from his abdominal incision site. He is diagnosed with an enterocutaneous fistula. The fluid loss from D.D.’s

fistula is about 600 mL/day. How will losses from D.D.’s fistula affect his PN?

Enterocutaneous (EC) fistulas are an abnormal communication between the

intestine and the skin. Most EC fistulas occur 7 to 10 days following surgery and are

classified by site of origin, output volume, etiology, and number of fistulas. Fluid,

electrolyte, and trace element losses from the EC fistula will vary depending on the

origin of the fistula. Losses must be accounted for and incorporated into the PN

formulation or replaced through a separate IV fluid infusion.

CASE 38-4, QUESTION 5: D.D. has stabilized and his physician would like to discharge him home in a few

days with the plan to continue TPN at home. D.D. is 5 feet 8 inches tall and weighs 141 lbs at discharge.

Design an appropriate PN therapy for home infusion.

Home TPN has allowed patients, such as D.D., to be discharged from the hospital

sooner. Candidates for home therapy must be physically and medically stable, have a

strong support network in the home setting to assist with care, and have an

appropriate home environment. They must be educated regarding the prescribed

therapy.

75

The first step in designing a PN regimen is to estimate energy and protein needs

(see Chapter 35, Basics of Nutrition and Patient Assessment). D.D. is 10 days out

from surgery, and his estimated requirements are 25 to 30 kcal/kg/day or

approximately 1,600 to 1,920 kcal/day. Protein goals must include adequate nitrogen

(protein) for wound healing and replacement for losses from the enterocutaneous

fistula. A goal of 1.5 to 1.8 g/kg/day (96–115 g) is reasonable. Long-term systemic

corticosteroid therapy is commonly seen in Crohn’s patients and may cause muscle

wasting. Losses of lean body mass from corticosteroids may increase amino acid

requirements.

To simplify his nutrition and fluid regimen, all of D.D.’s fluids, including

parenteral nutrients, electrolytes, vitamins, trace minerals, and water, should be

provided in one TNA container per day. D.D.’s home PN formulation can be

provided in 3,000 mL/day to meet maintenance requirements (see Case 38-1,

Question 5) and to replace losses from his enterocutaneous fistula (600 mL/day).

Nutrients provided include 100 g of amino acids (400 kcal); 264 g of dextrose (884

kcal); 50 g of lipid (500 kcal); and electrolytes, vitamins, and minerals to maintain

normal serum chemistries. Initially, daily intake and output must be monitored;

therapy should be adjusted based on this information and D.D.’s clinical status.

Adjustments in fluids and electrolytes may be needed. The fluids secreted by the

GI tract are rich in electrolytes, including sodium, potassium, chloride, and

bicarbonate. Measurement of the electrolyte content of the fistula fluid will determine

those that must be replaced, and in what quantities. Both fluid and electrolytes should

be replaced to prevent dehydration and electrolyte and acid–base imbalances.

In addition to losses of fluids and electrolytes, the trace element zinc is lost in

fluid from the small intestine. Approximately 12 mg of zinc is lost in each liter of

small bowel fluid, and should be replaced to prevent zinc deficiency. Furthermore,

zinc may play a role in wound healing.

76 Management of enterocutaneous fistulas may

include octreotide 50 to 100 mg given subcutaneously 2 or 3 times daily or added to

the parenteral nutrient formulation to decrease fistula output.

77

A home infusion pharmacy will be responsible for preparing D.D.’s PN

formulations. Typically, a seven day supply of PN therapy (7 bags) is prepared and

delivered to the patient’s home. These formulations must be refrigerated until

administration; however, formulations should be warmed to room temperature and

visually inspected for particulate matter before being administered. Because some

additives such as multivitamins are not stable for long periods, the patient or

caregiver must add these to the PN formulation just before administration.

Patients and caregivers preparing for home PN therapy must be taught how to

manage home therapy. This includes assessment of fluid status, care of a CVC,

infection, and the technical aspects of administering parenteral feeding

formulations.

75 Preparation for home PN includes placement of a central venous

access device for long-term TPN therapy.

7,8

CASE 38-4, QUESTION 6: What other measures can be used to simplify D.D.’s parenteral feeding regimen

and encourage ambulation?

Transitioning D.D. from a 24-hour continuous PN infusion to a cyclic infusion must

be considered. After D.D.’s PN regimen is formulated to meet his entire daily

nutrient and fluid needs and he is stable on that regimen, his PN regimen can then be

cycled. Cycling means that the PN formulation is infused for less than 24 hours per

day, so that there is time free from PN therapy each day. Cycling is usually done

gradually, prior to hospital discharge, and depends on the patient’s ability to tolerate

the changes in fluid and dextrose intake that occur when the TPN is started and

stopped each day. For example, the 24-hour PN infusion is decreased to a 20-hour

infusion (e.g., 8:00 PM to 4:00 PM) on cyclic PN day 1 and then the next day is

decreased to a 16-hour infusion (e.g., 8:00 PM to 12:00 noon), and the next day a 12-

hour infusion (e.g., 8:00 PM to 8:00 AM). With each incremental decrease in time, the

infusion rate should be increased such that the total PN volume is infused each day.

The infusion rate of the PN regimen is generally tapered up over 1 to 2 hours upon

PN initiation to avoid hyperglycemia and tapered down over 1 to 2 hours upon PN

discontinuation each day to avoid hypoglycemia. For example, a 16-hour cyclic PN

infusion with a 1-hour taper up and down can be calculated by taking the total TNA

volume divided by the infusion time minus 1 hour, to estimate the goal infusion rate.

The goal infusion rate is then divided by 2 to get the 1 hour taper up and taper down

rate. For D.D.’s 3,000 mL TNA, the regimen would start at 8:00 PM at 100 mL/hour

for 1 hour, then at 9:00 PM the rate would increase 200 mL/hour for 14 hours. At

11:00 AM the following day the TNA rate would taper back down to 100 mL/hour

and then at noon it would stop. Most infusion pumps used at home can automatically

make these adjustments in the infusion rate. Eventually, the nutrient formulation can

be infused for 10 to 12 hours during the night, leaving D.D. free from his PN infusion

during the day.

Vital signs, fluid intake and output, serum electrolytes, and glucose concentrations

should continue to be monitored. The serum glucose concentration should be

evaluated 30 minutes to 1 hour after the PN infusion is completed to be sure that

hypoglycemia does not occur.

CASE 38-4, QUESTION 7: In addition to his PN formula and ranitidine 150 mg IV, D.D. is receiving

hydrocortisone 100 mg IV every 8 hours, and he now needs insulin. Can these medications or any other

medications be mixed with his PN formula to simplify his medication regimen?

1.

2.

3.

4.

5.

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Patients receiving PN therapy often require concomitant drug therapy. Most

patients have adequate venous access or have multiple-lumen CVCs, so that mixing

medications with the parenteral nutrient formulation is not an issue. However, for

some patients with limited venous access, directly added medications or

piggybacking medications via a secondary infusion may be considered.

Although regular insulin, histamine type 2 (H2

)-receptor antagonists, and heparin

can be added to PN formulations in some circumstances, the routine addition of

medications to parenteral nutrient formulations is discouraged. Often times there are

requests to add other medications to a PN admixture. Specific criteria for drug

admixture with PN are listed below.

83

Stability and compatibility of the drug with the specific parenteral admixture over a

24-hour period must be determined before adding the medication.

The medication must have appropriate pharmacokinetics and proven efficacy for

continuous infusion.

The medication dose must have remained constant throughout the previous 24-hour

period before admixture in PN.

There should be a stable PN infusion rate for at least 24 hours before the

medication is added.

PN should include appropriate labeling to avoid pharmacotherapeutic problems

associated with abrupt discontinuation of PN.

CASE 38-4, QUESTION 8: After receiving home PN for 3 weeks, D.D.’s liver function tests are found to

be elevated. Current values are as follows:

Bilirubin, 0.8 mg/dL

Aspartate aminotransferase, 70 units/L

Alanine aminotransferase, 90 units/L

Alkaline phosphatase, 100 units/L

Could his PN be contributing to these abnormalities?

Elevations in liver function tests are common in adults receiving long-term PN

therapy and may be noted as early as 2 to 3 weeks after beginning therapy. The

abnormalities are usually mild and transient and do not progress to significant liver

dysfunction in adults. The predominant type of hepatobiliary dysfunction is steatosis

(fatty liver), whereas other patients develop cholestasis or cholelithiasis (biliary

obstruction). Liver-associated enzyme elevations usually resolve when PN therapy is

discontinued. Rarely does this dysfunction proceed to hepatic failure.

35,78

Other than avoiding overfeeding with carbohydrate and lipid, there are few

options to prevent or manage PN-associated liver abnormalities. Potential

management options include metronidazole and supplements of ursodeoxycholic acid,

choline, and carnitine. Transitioning to a lipid emulsion containing n-3 fatty acids

should also be considered. Patients with progressive liver disease may be candidates

for liver and small bowel transplantation.

78

The elevations in D.D.’s liver enzymes are not of concern at this time because they

are less than 3 times normal. However, since D.D. has been on home PN for 3 weks

and his wounds have healed, it is time to decrease his energy and protein intake to

maintenance requirements (20-25 kcal/kg/day and 0.8-1.0 g/kg/day of protein). Liver

enzymes should be monitored weekly. Because he may not need lifelong PN therapy,

the mild elevations are likely to resolve.

It is important to keep in mind that the liver is the primary organ involved with

digestion, metabolism, and storage of nutrients. When the functional capacity of the

liver is compromised (e.g., cirrhosis), macronutrient intolerance and imbalances may

occur. The patient may experience hyperglycemia, hypoglycemia, variations in blood

lipid levels, and accumulation of amino acid metabolites (ammonia).

CASE 38-4, QUESTION 9: After 10 months of receiving home TPN, D.D. suffers a fall and fractures his

wrist. Fracture of the wrist from a fall raises suspicions of compromised bone density. Subsequent DEXA scan

reveals a bone density T-Score of –3.1. Can these results be caused by long-term PN? What are other

complications of long-term parenteral therapy?

Long-term complications of PN are adverse effects associated with PN lasting

greater than 3 months. The most common complications include central catheter

complications (infection or occlusion), metabolic bone disease, and hepatobiliary

disease.

84

The exact cause of metabolic bone disease in long-term PN is unknown; however,

its origins appear to be multifactorial. The predominant risks factors for metabolic

bone disease in D.D. include Crohn’s disease, the medications used to manage it

(e.g., corticosteroids) coupled with the use of long-term PN therapy.

85 Both

osteoporosis and osteomalacia have been associated with long-term PN use.

Osteoporosis is the most common form of metabolic bone disease and is because of

loss of bone mass. Osteomalacia is the softening of bones and generally occurs as the

result of vitamin D deficiency. A combination of both osteoporosis and osteomalacia

may occur. Deficiencies in micronutrients such as calcium, magnesium, and vitamin

D are risk factors. Historically, bone abnormalities were thought to be caused by

aluminum toxicity. However, as aluminum has been nearly eliminated from TPNs,

metabolic bone disease remains an issue. High amino acid concentrations and TPN

cycling cause increased renal calcium excretion. Other factors include abnormalities

in the handling of calcium, phosphorus, and vitamins D and K.

Central catheter–related complications can vary from occlusion to central

catheter–related sepsis. Both of these complications are related to CVC care and are

a surrogate measure of overall catheter care.

86 Occlusion develops from fibrin and/or

lipid deposits. The consequences of catheter occlusion range from diminished flow

to complete occlusion necessitating removal of the catheter. Central catheter

infections are associated with the amount of times the catheter is accessed for PN

administration and blood sample removal. Patients with CVC infections usually

present with symptoms and signs such as pyrexia and tachycardia during PN infusion.

The causes of central catheter infections are bacterial and are usually because of skin

flora, Staphylococcus epidermis and Staphylococcus aureus. If CVC-related sepsis is

suspected, then the CVC being used should be discontinued and peripheral and

central cultures taken, while antimicrobial therapy is started pending culture results.

85

The incidence of hepatobiliary complications associated with long-term PN ranges

from 19% to 75%. These complications are variable, with patients experiencing

chronic elevations in liver enzymes to advanced liver disease (fibrosis and

cirrhosis). Liver disease associated with PN is termed intestinal failure–associated

liver disease (IFALD). IFALD is divided into nonnutrient and nutrient-related

causes. Nonnutrient causes of IFALD can include medications, biliary obstruction,

bacterial overgrowth, and intrinsic liver disease. Nutrient-related IFALD can be

caused by overfeeding, nutrient toxicities, and deficiencies. Nutrient toxicities

associated with IFALD include manganese, aluminum, and soybean oil. Some

nutrient deficiencies associated with IFALD are taurine, choline, carnitine, and

essential fatty acids. The most common histological finding in IFALD is steatosis

followed by cholestatic stasis, fibrosis, and finally cirrhosis. Hepatic steatosis is

associated with both under and overfeeding, so the importance of ensuring the correct

amount of calories is of utmost importance.

84

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KEY REFERENCES AND WEBSITES

A full list of references for this chapter can be found at

http://thepoint.lww.com/AT11e. Below are the key references and websites for this

chapter, with the corresponding reference number in this chapter found in parentheses

after the reference.

Key References

Driscoll DF. Intravenous lipid emulsions: 2001. Nutr Clin Pract. 2001; 16:215. (15)

Krzywda EA et al. Parenteral access devices. In: Gottschlich MM et al, ed. The Science And Practice Of

Nutrition Support: A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Publishing; 2001. (4, 37, 43, 49,

74, 75)

Kearns LR et al. Update on parenteral amino acids. Nutr Clin Pract. 2001;16:219. (19)

Mirtallo J et al. Safe practices for parenteral nutrition [published correction appears in J Parenter Enteral Nutr.

2006;30:177]. J Parenter Enteral Nutr. 2004;28:S39. (12)

Key Websites

American Society for Parenteral and Enteral Nutrition. http://www.nutritioncare.org.

http://www.nutritioncare.org/Library.aspx to access content for:

ASPEN Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and

enteral nutrition in adult and pediatric patients. JPEN J Parent Enteral Nutr. 2002;26(Suppl 1):1SA.

McClave SA et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill

patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition

(A.S.P.E.N.). JPEN J Parent Enteral Nutr. 2009;33:277.

COMPLETE REFERENCES CHAPTER 38 ADULT

PARENTERAL NUTRITION

Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition

in adult and pediatric patients [published correction appears in JPEN J Parenter Enteral Nutr 2002;26:144].

JPEN J Parenter Enteral Nutr. 2002;26(Suppl):1SA.

Dudrick SJ. History of parenteral nutrition. J Am Coll Nutr. 2009;28:243–251.

Dudrick SJ et al. Long-term parenteral nutrition with growth, development and positive nitrogen balance. Surgery.

1968;64:134.

Krzywda EA et al. Parenteral access devices. In: Gottschlich MM et al, ed. The Science and Practice of Nutrition

Support: A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Publishing; 2001:225.

Payne-James JJ, Kwahaja HT. First choice for total parenteral nutrition: the peripheral route. JPEN J Parenter

Enteral Nutr. 1993;17:468.

Kane KF et al. High osmolality feedings do not increase the incidence of thrombophlebitis during peripheral IV

nutrition. JPEN J Parenter Enteral Nutr. 1996;20:194.

Vanek VW. The ins and outs of venous access: part I. Nutr Clin Pract. 2002;17:85.

Vanek VW. The ins and outs of venous access: part II. Nutr Clin Pract. 2002;17:142.

Alhimyary A et al. Safety and efficacy of total parenteral nutrition delivered via a peripherally inserted central

venous catheter. Nutr Clin Pract. 1996;11:199.

[No authors listed]. ASHP Technical Assistance Bulletin on quality assurance for pharmacy-prepared sterile

products. Am J Hosp Pharm. 1993;50:2386.

Total parenteral nutrition/total nutrient admixture. USP DI Update. Rockville, MD: United States Pharmacopeial

Convention; 1996:66.

Mirtallo J et al. Safe practices for parenteral nutrition [published correction appears in JPEN J Parenter Enteral

Nutr. 2006;30:177]. JPEN J Parenter Enteral Nutr. 2004;28:S39.

Goulet O et al. A new intravenous fat emulsion containing soybean oil, medium chain triglycerides, olive oil, and

fish oil: a single-center, double-blind randomized study on efficacy and safety in pediatric patients receiving

home parenteral nutrition. JPEN J Parenter Entern Nutr. 2010;34:485–495

Reimund JM et al. Efficacy and safety of an olive oil-based intravenous fat emulsion in adult patients on home

parenteral nutrition. Aliment Pharmacol Ther. 2005;21:445–454.

Driscoll DF. Intravenous lipid emulsions: 2001. Nutr Clin Pract. 2001;16:215.

Marchesini G et al. Nutritional treatment with branched chain amino acids in advanced liver cirrhosis. J

Gastroenterol. 2000;35(Suppl 12):7.

Fabbri A et al. Overview of randomized clinical trials of oral branched-chain amino acid treatment in chronic

hepatic encephalopathy. JPEN J Parenter Enteral Nutr. 1996;20:159.

Skeie B et al. Branch-chain amino acids: their metabolism and clinical utility. Crit Care Med. 1990;18:549.

Kearns LR et al. Update on parenteral amino acids. Nutr Clin Pract. 2001;16:219.

Brown RO, Compher C. A.S.P.E.N. clinical guideline: nutrition support in adult acute and chronic renal failure.

JPEN J Parenter Enteral Nutr. 2010;34(4):366–377.

McClave SA et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill

patient. Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition. JPEN J

Parenter Enteral Nutr. 2009;33:277–316.

Melnick G. Value of specialty intravenous amino acids solutions. Am J Health Syst Pharm. 1996;53:671–674.

Neyra R et al. Increased resting energy expenditure in patients with end-stage renal disease. JPEN J Parenter

Enteral Nutr. 2003;27:36–42.

Scheinkestel CD et al. Impact of increasing parenteral protein loads on amino acid levels and balance in critically

ill anuric patients on continuous renal replacement therapy. Nutrition. 2003;19:733–740.

Scheinkestel CD et al. Prospective randomized trial to assess caloric and protein needs of critically ill, anuric,

ventilated patients requiring continuous renal replacement therapy. Nutrition. 2003;19:909–916.

Fiaccadori E et al. Effects of different energy intakes on nitrogen balance in patients with acute renal failure: a

pilot study. Nephrol Dial Transplant. 2005;20:1976–1980.

Cano N et al. ESPEN guidelines on enteral nutrition: adult renal failure. Clin Nutr. 2006;25:295–310.

Kopple J. The National Kidney Foundation K/DOQI clinical practice guidelines for dietary protein intake for

chronic dialysis patients. Am J Kidney Dis. 2001;38(4 Suppl 1):S68–S73.

Blumenkrantz MJ et al. Metabolic balance studies and dietary protein requirements in patients undergoing

continuous ambulatory peritoneal dialysis. Kidney Int. 1982;21:849–861.

Bayer-Berger M et al. Incidence of phlebitis in peripheral parenteral nutrition: effect of the different nutrient

solutions. Clin Nutr. 1989;8:81.

Daly JM et al. Peripheral vein infusion of dextrose/amino acid solutions ± 20% fat emulsion. JPEN J Parenter

Enteral Nutr. 1985;9:296.

Driscoll DF. Clinical issues regarding the use of total nutrient admixtures. DICP. 1990;24:296.

Wolfe RR. Glucose metabolism in burn injury: a review. J Burn Care Rehabil. 1985;6:408.

Delafosse B et al. Respiratory changes induced by parenteral nutrition in postoperative patients undergoing

inspiratory pressure support ventilation. Anesthesiology. 1987;66:393.

Quigley EM et al. Hepatobiliary complications of total parenteral nutrition. Gastroenterology. 1993;104:286.

Seidner DL et al. Effects of long-chain triglyceride emulsions on reticuloendothelial system function in humans.

JPEN J Parenter Enteral Nutr. 1989;13:614.

Matarese LE. Metabolic complications of parenteral nutrition therapy. In: Gottschlich MM et al, ed. The Science

and Practice of Nutrition Support: A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Publishing;

2001:269.

Solomon SM, Kirby DK. The refeeding syndrome: a review. JPEN J Parenter Enteral Nutr. 1990;14:90.

Brooks MJ, Melnik G. The refeeding syndrome: an approach to understanding its complications and preventing its

occurrence. Pharmacotherapy. 1995;15:713.

Mowatt-Larssen CA, Brown RO. Specialized nutritionalsupport in respiratory disease. Clin Pharm. 1993;12:276.

Talpers SS et al. Nutritionally associated increased carbon dioxide production. Excess total calories vs high

proportion of carbohydrate calories. Chest. 1992;102:551.

Sacks GS, Mouser JF. Is IV lipid emulsion safe in patients with hypertriglyceridemia? Nutr Clin Pract.

1997;12:120.

Barber JR et al. Parenteral feeding formulations. In: Gottschlich MM et al, ed. The Science and Practice of

Nutrition Support: A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Publishing; 2001:251.

Driscoll DF. Total nutrient admixtures: theory and practice. Nutr Clin Pract. 1995;10:114.

Centers for Disease Control and Prevention. Guidelines for the prevention of intravascular catheter-related

infections. MMWE. 2002;51(No. RR-10):1–28

D’Erasmo E et al. Serum albumin level at admission: mortality and clinical outcome in geriatric patients. Am J

Med Sci. 1997;314:17–20.

Choban PS et al. Nutrition support of obese hospitalized patients. Nutr Clin Pract. 1997;12:149.

Choban PS, Dickerson RN. Morbid obesity and nutrition support: is bigger different? Nutr Clin Pract.

2005;11:300–311.

Seidner DL, Fuhrman MP. Nutrition support in pancreatitis. In: Gottschlich MM et al, ed. The Science and

Practice of Nutrition Support: A Case-Based Core Curriculum. Dubuque, IA: Kendall/Hunt Publishing;

2001:553.

Singer P et al. ESPEN guidelines on parenteral nutrition: Intensive care. Clin Nutr. 2009;28:387–400.

Lewis KS et al. Intensive insulin therapy for critically ill patients. Ann Pharmacother. 2004;38:1243–1251.

McMahon MM. Management of hyperglycemia in hospitalized patients receiving parenteral nutrition. Nutr Clin

Pract. 1997;12:35.

van den Berghe G et al. Intensive insulin therapy in the critically ill patients. N EnglJ Med. 2001;345:1359.

McMahon MM et al. ASPEN clinical guideline: nutrition support of adult patients with hyperglycemia. JPEN J

Parenter Enteral Nutr. 2013;37(1):23–36

Montori VM et al. Hyperglycemia in acutely ill patients. JAMA. 2002;288:2167.

McMahon MM, Rizza RA. Nutrition support in hospitalized patients with diabetes mellitus. Mayo Clin Proc.

1996;71:587.

Federal Register. April 20, 2000 (Volume 65, Number 77).

Task Force for the Revision of Safe Practices for Parenteral Nutrition. Safe practices for parenteral nutrition.

JPEN J Parenter Enteral Nutr. 2004;28:S54.

Baumgartner TG. Enteral and parenteral electrolyte therapeutics. Nutr Clin Pract. 2001;16:226.

Brown KA et al. A new graduated dosing regimen for phosphorus replacement in patients receiving nutrition

support. JPEN J Parenter Enteral Nutr. 2006;30:209.

Rosen GH et al. Intravenous phosphate repletion regimen for critically ill patients with moderate

hypophosphatemia. Crit Care Med. 1995;23:1204.

Mizock BA. Alterations in carbohydrate metabolism during stress: a review of the literature. Am J Med.

1995;98:75.

Rosemarin DK et al. Hyperglycemia associated with high, continuous infusion rates of total parenteral nutrition

dextrose. Nutr Clin Pract. 1996;11:151.

van den Berghe G et al. Outcome benefit of intensive insulin therapy in the critically ill: insulin dose versus

glycemic control. Crit Care Med. 2003;31:359.

Furnary AP et al. Continuous intravenous insulin infusion reduces the incidence of deep sternal would infection in

diabetic patients after cardiac surgical procedures. Ann Thorac Surg. 1999;67:352.

Zerr KJ et al. Glucose control lowers the risk of wound infection in diabetics after open heart operations. Ann

Thorac Surg. 1997;63:356.

Rose BD. Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th ed. New York, NY: McGraw-Hill;

1994:891.