July 2011 Issue
Optimizing Care in Home Parenteral Nutrition — The RD’s Role
By Theresa A. Fessler, MS, RD, CNSC
Vol. 13 No. 7 P. 38
Home parenteral nutrition (HPN) is a life-saving therapy for many people whose gastrointestinal (GI) tract is nonfunctional. Current demographic information is lacking, but data from the 1990s indicated there were an estimated 40,000 people on HPN in the United States.1
The American Society for Parenteral and Enteral Nutrition has published standards for the multidisciplinary care of home patients who require specialized nutrition support.2 Interdisciplinary collaboration among physicians, nurses, dietitians, pharmacists, and patients is required for successful outcomes.
RDs are essential for improving HPN care and outcomes through active involvement in determining medical necessity and the goals of therapy, managing electrolyte and hydration status, monitoring for signs of infection, and providing nutritional management of long-term issues such micronutrient status and liver and bone health.
Medical Necessity and Financial Coverage
Prior to initiating HPN, it must be determined whether PN is medically necessary. The importance of this step cannot be overemphasized. HPN carries significant risks (both catheter-related and metabolic complications)3 and is very costly, with charges in the range of $300 to $400 per day. Efforts should be made to use the GI tract whenever possible.
It must also be determined whether HPN is covered by a patient’s medical insurance. Medical insurance companies typically preauthorize based on a physician’s evaluation of necessity. Medicare covers 80% of approved costs, but if its specific criteria are not met, complete denial of coverage can result, even long after HPN has been initiated. Patients must have a nonfunctional bowel with an anticipated need for PN for three months or longer. In certain cases, a trial of enteral feeding is required to prove intolerance. The RD’s review of medical records for diagnosis, surgical procedures, GI anatomy, the length of the remaining bowel, radiologic evidence of GI dysmotility or obstruction, medications used, attempts for enteral feeding, laboratory data, and evidence of malnutrition will help determine and prove a patient’s need for HPN. (The article “Medicare Reimbursement of Home Nutrition Support” by Mike Nelson, RD, CNSD, published in the January 2007 issue of Today’s Dietitian, includes a thorough discussion about Medicare coverage of HPN.)
For every new patient who starts on HPN, it is important to know the physician’s and/or surgeon’s goals and the patient’s desires. For example, a patient with major organ dysfunction or one who is very malnourished and at risk of refeeding syndrome will require more frequent monitoring and formula changes. In end-of-life situations, PN will need to be discontinued at some point because it can contribute to discomfort and stress for both patients and their caregivers.
Questions to ask include the following:
• Will PN be permanent or will the patient be able to transition to an oral diet?
• Does the patient need to gain, lose, or maintain weight?
• Does the patient have specific risks?
• Is future surgery planned?
• What is the patient’s prognosis?
Monitoring During HPN
Monitoring PN in the home is very different from monitoring it in the hospital. Home care RDs need to communicate with patients, family members, nurses, care coordinators, discharge planners, social workers, physicians, pharmacists, and others, mostly by phone and e-mail. Lab data and medical information is faxed by other healthcare workers or is available on computerized medical charts. Unlike in the hospital setting where PN is mixed daily and changed often, HPN is usually made in one-week batches. RDs should change the nutrient content of PN only when necessary, as frequent adjustments are neither possible nor practical.
The chemistry profile, liver function tests, and complete blood count are typically done once per week initially. After the patient has been stable for several weeks, the frequency of lab tests can be decreased to one to two times per month.4
Glucose levels reported in the chemistry profiles of patients with diabetes will not always reflect overall glucose control. Blood is typically drawn in the daytime, and most patients infuse their HPN during the night. Patients or caregivers should initially check glucose levels before, during, and after the PN cycle and can decrease the frequency of checking when patients are stabilized. Regular insulin can be added to PN for stable diabetic patients.
Fluid and Electrolyte Management
The home care RD must be knowledgeable and experienced in the area of fluid and electrolyte issues to effectively manage patients on HPN. Laboratory data alone are not sufficient, as electrolyte levels must be evaluated along with physical information to be accurately interpreted.5 Asking patients questions about thirst, urine output, swelling/fluid retention, weight changes, and symptoms of weakness or feeling faint helps clarify fluid and electrolyte status. Asking the home nurse about a patient’s heart rate, blood pressure, and presence of edema is also helpful.
Patients at risk for refeeding syndrome, those with GI fluid losses, and patients with renal failure will need more frequent electrolyte monitoring and are more likely to require the adjustment of electrolyte content of PN. Patients with refeeding syndrome will need to have PN calories gradually increased over a period of days or weeks. Ideally, patients are stabilized on PN in the hospital prior to discharge. Initiation of PN in the home setting is more complex. Readers desiring more information should refer to the article “Home Initiation of Parenteral Nutrition,” published in 2007 in Nutrition in Clinical Practice.
Loss of excessive gastric fluid can result in hyponatremia, metabolic alkalosis, and dehydration. Excessive loss of ileostomy or small bowel fistula drainage can result in hyponatremia, low magnesium levels, dehydration, and metabolic acidosis.5,6 In some cases, additional separate IV fluid may be necessary. While both IV fluids and PN are used in the hospital, IV fluids are usually not used at home. Thus, whenever possible, the healthcare team should ensure that patients are stabilized with adequate fluid in PN prior to their discharge from the hospital. In some cases, home patients should actually measure and record outputs (including urine) to help ensure that intake from HPN will meet their needs. When outputs stabilize, patients can stop measuring them.
PN-Associated Liver Disease
The risk of PN-associated liver disease (PNALD) is connected to short bowel (less than 50 cm), a lack of enteral stimulation resulting in biliary sludge, and episodes of sepsis and small bowel bacterial overgrowth, which have toxic effects on the liver. Overfeeding, continuous PN infusion, the type and amount of lipid (long-chain omega-6 fatty acids) used, and the lack of choline and carnitine in PN have also been identified as possible etiologic factors.
Elevations in aminotransferase levels can indicate steatosis, or fat accumulation, in the liver. Steatosis can progress to fibrosis or cirrhosis for patients on long-term HPN. Elevations in alkaline phosphatase and serum bilirubin are an indication of cholestasis, which is more serious and can progress to cirrhosis and liver failure. Elevation in alkaline phosphatase is not specific to hepatobiliary disease but occurs in PN-associated cholestasis.7
RDs can take several actions to prevent and manage PNALD. Avoiding overfeeding (both dextrose and lipid) and infusing PN on a cyclic basis (eg, 10 to 14 hours per day) rather than continuously are two of the simplest ways to prevent PNALD. Decreasing IV lipid in PN to 1 g/kg or less is also helpful. Oral or enteral intake should be maximized (when possible) to stimulate bile flow, and RDs should routinely reevaluate patients’ ability to take oral or enteral nutrition. Physicians can order medications to stimulate bile flow, such as ursodiol (ursodeoxycholic acid). Carnitine can be supplemented orally in some patients or L-carnitine (for injectable use) can be added to PN. This practice makes sense in theory but has not been proven to improve liver function in adults. Parenteral choline has been shown to help resolve steatosis in adults on long-term PN. However, it is currently not available on the market for general use in PN. Other actions include vigilance on the part of the patient and healthcare team to avoid catheter-related bloodstream infections and to promptly identify and treat cases of intestinal bacterial overgrowth.
Patients on HPN are at risk for toxicities or deficiencies of some trace elements. The RD should be aware of the symptoms and periodically monitor blood levels. Current combination trace element products provide five times (or more) the amount of manganese and twice the amount of copper per daily dose than the current recommended parenteral requirements. Many patients on long-term PN develop elevated blood levels of manganese, usually without symptoms, yet symptomatic manganese toxicity has been reported in several cases. Symptoms include Parkinsonlike tremor and gait disorders, confusion, and headache. Patients with cholestasis are expected to develop elevated manganese and copper levels, since these elements are excreted via the biliary tract. However, hypermanganesemia has been reported in many patients with normal liver function. PN also contains contaminant manganese and chromium. Patients on HPN have elevated chromium levels, but no cases of actual chromium toxicity have been published. More information on parenteral trace element use and monitoring is available.8
Patients on HPN are likely to become iron deficient because PN typically used in the United States contains no iron due to incompatibilty with IV lipid and because of a very low risk of anaphylactic reaction with iron dextran. However, some practitioners do order small amounts of iron in lipid-free PN (and iron is used in PN in Europe). It is important to be aware of whether a PN formula contains iron, since the parenteral route bypasses the normal GI homeostatic mechanism that prevents toxicity. If a patient is deficient, oral iron is safest, but if this route of administration is not possible, separate IV iron infusions are necessary.8
Catheter sepsis is the most common catheter-related complication in HPN. The RD can help manage this by routinely questioning patients about the presence of fever or chills and monitoring lab reports for elevations in white blood cell count. If signs or symptoms are present, the patient’s physician and home RN should be notified promptly. Typically, blood cultures—both peripheral and from the central line—are ordered.3
Long-term PN therapy is associated with an increased risk of developing metabolic bone disease.9 Patients with a history of GI disease, steroid medication use, vitamin D deficiency, or malnutrition in general are already at risk of osteopenia or osteoporosis. Inactivity, low body weight, advanced age, and lack of sunlight exposure increase that risk. PN itself can contribute to the problem if it contains inadequate calcium and phosphorus; if it contains excessive amounts of amino acids and/or sodium, which are theorized to increase calcium excretion; and because of aluminum contamination.9,10
HPN should provide adequate calcium (15 mEq/day) and phosphorous (15 mMol/day). Avoid excessive sodium unless necessary to offset GI or renal sodium losses. When patients have achieved nutritional repletion, RDs should ensure that PN provides 1 to 1.5 g of protein per kilogram of body weight per day. They should monitor serum bicarbonate levels, as renal or GI losses can result in metabolic acidosis and subsequent loss of calcium and phosphorus from bone as a buffering system. Acetate should be increased in PN in the situation of metabolic acidosis.9 Patients should engage in weight-bearing exercise if possible to help maintain bone density.
Many patients on HPN are deficient in vitamin D. Since there is no single parenteral vitamin D product currently available, patients can take high-dose oral vitamin D if they have sufficient small bowel to absorb at least some of it.11 For those who do not have sufficient bowel, sunlight exposure is one of the only remaining sources but is unreliable for those who live in latitudes far from the equator, especially during the winter. Sunlamp products are available (www.sperti.com) but are costly, and medical insurance is unlikely to cover them.
The aluminum content of PN solutions should be minimized, with an “ideal” goal of 4 to 5 mcg/kg/day, but meeting this goal is not always possible for patients with a low BMI. All of the components of PN contain varied amounts of contaminant aluminum, which is known to increase with longer time in storage, as it leaches from glass containers. Calcium gluconate, potassium and sodium phosphate salts, and trace mineral additives are high in contaminant aluminum. Aluminum binds to transferrin, and transferrin with iron bound to it has less affinity for aluminum.10
Quality of Life and Psychosocial Issues
Patients on HPN must deal with difficult and inconvenient problems, such as the tasks involved in preparing the PN for infusion, the annoyance of being connected to the pump and length of the feeding cycle, interference with their social life, diarrhea or unpleasant ostomy or fistula drainage, and the expense. Some patients may worry about bloodstream infection and their disease process and outcome. Some are unable to eat or they eat much less than normal. Some are dealing with end-of-life issues.
RDs must be aware of these issues when speaking to patients and their caregivers. They must treat these individuals in a sensitive and considerate manner and take their individual goals, priorities, and expectations into account.12 Smith et al showed that involvement with a national support group actually improves outcomes in terms of quality of life, depression, and incidence of catheter-related infections.13 The RD can provide patients and caregivers with information about the Oley Foundation national support group (www.oley.org).
RDs Can Make a Positive Impact
Working with patients on HPN to promote successful outcomes can be a challenging and rewarding experience for RDs. Providing optimal care for patients on HPN requires RDs to have a working knowledge of and experience with determining the medical need for PN, establishing goals of care, and managing fluids and electrolytes, appropriate diet advancement (when possible), and long-term PN complications.
— Theresa A. Fessler, MS, RD, CNSC, is a nutrition support specialist at the University of Virginia Health System in Charlottesville and a freelance writer.
Common Indications for Home Parenteral Nutrition
• Severe short bowel syndrome—insufficient enteral absorptive capacity
• Complete small bowel obstruction that cannot be surgically corrected
• Partial bowel obstruction with failure of enteral tube feeding
• Malnutrition with malabsorption that has not improved with the use of medications or altered nutrient content of enteral formulas
• Malnutrition and motility disorder that has not improved with medications
• High output enterocutaneous fistula with inability to enterally feed distal to it
• Inability to maintain nutrition/hydration due to high ostomy output that has not improved with the use of medications
— Adapted from Nelson M. Medicare reimbursement of home nutrition support. Today’s Dietitian. 2007;9(1):12-21.
Fluid Imbalance: Some Physical Signs and Symptoms in Home Care
• Rapid weight loss
• Orthostatic hypotension
• Low blood pressure
• Decreased skin turgor
• Decline in frequency and volume of urine
• Dark color of urine
• Excessive urine volume
• Edema, swelling
• Rapid weight gain
— Adapted from references 5 and 6
1. DeLegge MH. Demographics of home parenteral nutrition. JPEN J Parenter Enteral Nutr. 2002;26(5 Suppl):S60-S62.
2. Kovacevich DS, Frederick A, Kelly D, et al. Standards for specialized nutrition support: Home care patients. Nutr Clin Pract. 2005;20(5):579-590.
3. Howard L, Ashley C. Management of complications in patients receiving home parenteral nutrition. Gastroenterology. 2003;124(6):1651-1661.
4. DeLegge MH, Ireton-Jones C. Home care. 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: 725-739.
5. Pemberton LB, Pemberton DK, Cuddy PG. Treatment of Water, Electrolyte, and Acid-Base Disorders in the Surgical Patient. Columbus, Ohio: McGraw-Hill; 1994.
6. Langley G. Fluid, electrolytes and acid-base disorders. 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: 104-128.
7. Kumpf VJ. Parenteral nutrition-associated liver disease in adult and pediatric patients. Nutr Clin Pract. 2006;21(3):279-290.
8. Fessler TA. Trace element monitoring and therapy for adult patients receiving long-term total parenteral nutrition. Practical Gastroenterology. 2005;29(3):44-65. Available at: http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/FesslerArticle.pdf
9. Ferrone M, Geraci M. A review of the relationship between parenteral nutrition and metabolic bone disease. Nutr Clin Pract. 2007;22(3):329-339.
10. Gura KM, Puder M. Recent developments in aluminum contamination of products used in parenteral nutrition. Curr Opin Clin Nutr Metab Care. 2006;9(3):239-246.
11. Boullata J, Compher C, Schiavone P, Stoner N, Hoff K, Kinosian B. Oral vitamin D repletion in patients with parenteral nutrition dependent intestinal failure. Nutr Clin Pract. 2009;24(1):138.
12. Winkler MF, Hagan E, Wetle T, Smith C, O’Sullivan Maillet J, Touger-Decker R. An exploration of quality of life and the experience of living with home parenteral nutrition. JPEN J Parenter Enteral Nutr. 2010;34(4):395-407.
13. Smith C, Curtas S, Werkowitch M, Kleinbeck SV, Howard L. Home parenteral nutrition: Does affiliation with a national support and educational organization improve patient outcomes? JPEN J Parenter Enteral Nutr. 2002;26(3):159-163.