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Principles and Strategies for Monitoring Home Parenteral NutritionNutrishare, Inc, Elk Grove, California Correspondence: Correspondence: John Siepler, Research Specialist, Nutrishare, Inc, 10519 East Stockton Boulevard, Suite 110, Elk Grove, CA 95624. Electronic mail may be sent to john{at}nutrishare.com. Patients who cannot ingest adequate calories to maintain body weight via their gastrointestinal tract may require parenteral nutrition (PN) at home. As with any therapy, the patient must be evaluated to determine if the home PN (HPN) is effective and the patient is free of complications. This review discusses specific items to monitor for HPN patients. Parameters to monitor can be divided into those used to determine effectiveness and those used to prevent complications of HPN. In addition, potential HPN-associated complications can be divided into those that occur with short- or long-term PN administration. Specific items to monitor are discussed within this framework. Parenteral nutrition (PN) is complex and can be lifesaving in certain patients. One group of patients who may benefit from PN use includes those who have an inability to tolerate adequate oral nutrition to maintain their body mass. For these patients, home PN (HPN) is a realistic option. Other patients who may benefit from HPN include those with an inadequate bowel length or patients with inadequate bowel motility. Many patients with short bowel syndrome (SBS) or motility disorders are likely to require HPN for prolonged periods of time (often years and sometimes lifelong). Other patients may require HPN for shorter periods of time due to a clinical condition that does not allow oral nutrition. Patients who require short-term HPN courses may include those with pancreatitis (in patients unable to tolerate nasojejunal feeding), enterocutaneous fistulae, and any other condition where feeding via the gastrointestinal (GI) tract would be considered contraindicated. This review will discuss the monitoring of HPN patients, presenting the evidence for specific items to monitor to ensure efficacy or to prevent complications. Although it is tempting to add treatment modalities to cure the clinical conditions that these monitoring parameters indicate, a detailed discussion of treatment is out of the scope of this article.
The American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) has published standards of practice for specialized nutrition support for home care patients.1 These standards stress the multidisciplinary nature of managing a HPN patient. A very important area is the education of the HPN patient to perform the necessary tasks appropriately. Besides recognizing the potential problems with HPN, the patient must be a partner in the assessment for efficacy and prevention of complications. The patient should be aware of the need to obtain appropriate laboratory tests but must also be able to recognize signs and symptoms of complications. These may be related to HPN use but are also associated with the vascular access device (VAD) necessary for infusion of the HPN. If the goal of monitoring HPN patients is to assure efficacy, as well as prevent and identify HPN-associated complications. The clinician and the patient should evaluate each of the parameters monitored in the context of his or her medical condition. Because accurate monitoring may result in changes in patient management, the complete patient must be considered rather than reacting to only one abnormal monitoring parameter. With regard to the incidence of HPN-associated complications, Messing and Joly2 recently summarized the HPN literature suggesting that HPN-associated complications occur at about 2% per year. The authors stress that specific nutrition outcomes and goals should be devised before initiating HPN, and monitored regularly during the course of therapy. The progress of the HPN patient should be periodically reevaluated to determine if the predetermined outcomes are achieved. Adequate laboratory tests should be obtained on a regular basis to determine electrolyte and glucose tolerance. In addition, more laboratory investigation should be used to determine intravenous (IV) lipid tolerance, liver function, and bone mineral density. The following is a review of the monitoring parameters for HPN patients.
It is extremely important to involve the HPN patient in setting goals for nutrition support because the patient is the one infusing the HPN, has a central VAD, and is exposed to numerous potential adverse reactions. Goals should include objective parameters such as optimal weight and improvement in primary disease but also subjective factors such as the ability to perform normal activities of daily living and a feeling of self-worth. To evaluate the efficacy of PN, one must monitor the patient for changes in underlying disease, body weight, laboratory tests, and other parameters (Table 1).
Improvement in Primary Disease
Weight Once the goal weight is set, it should be recorded at every clinic visit. If clinic visits are infrequent, a telephone call to the patient should be performed monthly to record the current weight and whether the patient is satisfied with the weight. This weight should be obtained using the same scale and at the same time of the day for each documentation. This simple task may be the best way to determine if calories provided in the HPN are appropriate, insufficient, or excessive.
Activities of Daily Living If improvement in strength is a goal, monitoring strength is desirable. Objective measures of strength such as hand-grip strength have been studied in institutional settings but have not been evaluated extensively in the home care environment. At each clinic visit and during telephone communication, questions must be asked to determine patient tolerance of routine daily activities. The patient must be reminded that improvement may be slow, but if the nutrition plan is effective, the activity goals are possible to achieve.
Laboratory Values and Tests There are numerous methods to determine calorie requirements. Jeppesen and Mortensen5 from Denmark determine the intestinal absorption of nutrients for each patient. This test is conducted by having the patient ingest an oral diet of known calories and protein. This is compared with analysis of stool and urine output for the calories and protein using bomb calorimetry and analysis for nitrogen. Although calorie requirements are determined in a scientific fashion, this practice is quite labor intensive and is not widespread. Even the best efforts to estimate calorie requirements may not produce the desired clinical response. One confounding factor is compliance, which may be a problem with HPN. Patients frequently fail to infuse the entire HPN formulation. This may occur when the patient infuses less than the prescribed HPN formulation or skips infusions. If the patient asks the home infusion company to deliver less than the prescribed number of HPN formulations on a routine basis, this might be an indication of this practice. If the patient discards the HPN formulation rather than infusing it, the practice may be more difficult to detect. In this case, the patient may continue to order HPN as prescribed but not order the infusion sets to administer the HPN formulation. Occasionally, the patient may deny the practice even when confronted by the clinician, but careful and sensitive questioning can usually uncover the practice. Ultimately, the patient must be a partner in planning nutrition goals. If the patient agrees with the nutrition goals, it is likely the practice of underinfusing HPN will be decreased.
HPN-associated complications can be divided into 2 general categories: short- and long-term. For the purpose of this review, short-term complications are defined as those occurring within 30 days of initiation of HPN. Those occurring after 30 days are defined as long-term complications. Parameters to monitor for short- and long-term complications are summarized in Tables 2 and 3.
The American Gastroenterological Association published a technical review of PN, reporting an overall complication rate of 13%–20%.6 This estimate was based on data primarily collected in hospitalized patients. A more realistic estimate in patients receiving HPN would be approximately 2% per year.2 Howard7 reviewed the OLEY Foundation database in 1996 and in again in 2006 to determine the incidence of HPN-associated complications. The author reported complication rates categorized by underlying disease, finding a rate of 0.8%–2.1% per patient year. The economic cost of these complications has been estimated to be in excess of $100,000/patient year. Ugur and associates8 reviewed HPN use in Denmark between 1996 and 2001, reporting the incidence of mortality, catheter-related bacteremia, and catheter occlusion to be <0.4/1000 HPN-days. Several European studies have estimated complications at a lower rate than those published in the United States. A direct comparison with U.S. data is difficult due to different definitions of complications, data collection methods, and different usage patterns of HPN between countries.
Dehydration Many patients who require HPN have SBS, and by definition, bowel length and surface area are inadequate for sufficient absorption of nutrients. In addition, stool output is frequently high, which may complicate maintenance of adequate hydration and can lead to intravascular dehydration. Thus, many of these patients have difficulty in maintaining adequate hydration. Symptoms typical of dehydration include postural hypotension, dry mucous membranes, decreased skin turgor, or a concentrated, decreased volume of urine. This can be complicated by increased insensible fluid losses that can occur, especially in the summer when the weather is warm. In addition to the signs and symptoms noted above, serum sodium (Na) and sometimes chloride (Cl) will increase with free water depletion. See the section on electrolyte abnormalities for more discussion on this topic. Periodic dehydration in HPN patients may seem like a minor problem, but Lauverjat and associates9 found decreased renal function in 52% of long-term HPN patients. Most of these cases were associated with dehydration complicated by large intestinal fluid losses. An elevation in blood urea nitrogen (BUN) and an inversion of the urinary sodium/potassium (Na/K) values were the only abnormal monitoring parameters. Monitoring BUN and creatinine (Cr) was recommended, and if these values were abnormal, urinary Na/K concentrations were suggested to further confirm the presence of dehydration. In these cases, additional IV fluid or oral rehydration salts can be successful in reversing the condition.10
Catheter Malposition and Thrombosis Although the catheter tip position is verified at insertion, the tip may become dislodged and migrate afterwards. The exact incidence of catheter malposition is unknown, but it is most likely <5%.11,12 Symptoms of a malpositioned catheter depend on the location of the tip. If the catheter tip migrates up into the jugular vein, the patient can experience a headache and increased swelling on 1 side of the face during HPN infusion. Although this symptom is consistent with superior vena cava syndrome, if a catheter malposition is suspected, the patient should be referred to have the catheter tip position reevaluated. If a malposition is confirmed, the catheter must be repositioned or replaced with a new one. Occlusion of a VAD can occur from thrombus formation, lipid occlusion, or mineral precipitation (usually calcium phosphate). The catheter occlusion rate of implanted VADs (18% of which were used for HPN) in a group of oncology patients was 0.8/1000 catheter-days,2,13,14 although a lower rate is a more realistic estimate for HPN patients. Any catheter occlusion is significant in a HPN patient because resolution may require replacement of the catheter. Frequent catheter replacement can be associated with loss of viable catheter sites. The first indication of occlusion may be an increased resistance when flushing the catheter or difficulty in withdrawing blood. Difficulty in blood withdrawal from the catheter may be the result of a "thrombus flap" that covers the catheter tip. Although infusion of HPN occurs in a routine fashion, the flap covers the catheter tip on blood withdrawal and occludes the catheter. These events can occur even though the HPN infusion pump does not alarm in response to increased backpressure. Thorough treatment guidelines for management of a catheter-associated thrombus are beyond the scope of this paper. Examples of treatment options include alteplase for acute resolution of a suspected thrombus. If alteplase fails, other options are available to clear lipid or calcium-phosphorus occlusions. If the occlusion persists, the catheter may need to be replaced. Low-dose warfarin (1 mg daily) has been successfully used for prophylaxis of catheter-related thrombosis.15
Catheter-Related Infections Catheter infections can be divided into 2 general categories: CRBSI and exit-site infections. Of the 2 types, CRBSI are the more serious, with an incidence of 0.2–5 per 1000 catheter-days5 in HPN patients. In addition, there is a perception that there may be a difference in CRBSI rate, depending on catheter type.17 In a recent study, inpatients receiving PN were evaluated and overall complications requiring removal of the catheter were significantly greater in those patients with subclavian vs PICC lines. This may have occurred because replacement of a PICC line is easier than an implanted catheter, as the infection rate was not significantly different between the 2 types of catheters. In another study, tunneled central catheters used in oncology patients found a CRBSI rate of 1.76/1000 catheter-days.13 Symptoms of CRBSI in HPN patients include fever and chills at the time of HPN infusion. In fact, any fever in a HPN patient should be considered significant and should be evaluated promptly. A blood culture collected through the VAD, accompanied by a second peripherally obtained culture, is the appropriate method to confirm a CRBSI. Treatment should be initiated promptly as a significant delay in treatment may result in systemic infectious complications. Antimicrobials and sometimes removal of the VAD are required for treatment of CRBSI. However, frequent catheter replacement may result in a loss of viable placement sites for future catheters. The reader is referred to other published reviews for further in-depth information on the management of CRBSIs.18,19
Electrolyte Abnormalities Na and Cl. Abnormalities of Na and Cl are often associated with changes in hydration status. In the HPN patient with SBS, excessive loss of free water through insensible losses, stool, or urine can result in an increase of serum Na and Cl. Sodium content of ileostomy output may be in the range of 80–100 mEq/L, with potassium content being 10–20 mEq/L.20 These numbers are estimates based on several studies; thus, for difficult patients, an electrolyte analysis of stool or ostomy output may be required. With the presence of high stool or ostomy output, the patient may have symptoms of dehydration manifesting as postural hypotension and oliguria (ie, decreased urine volume). Many patients also have increases in blood levels of hemoglobin (Hgb), hematocrit (Hct), BUN, and Cr. These changes can occur rapidly, sometimes in <24 hours if stool or ostomy output is high. If an HPN patient has symptoms of dehydration, obtaining a basic metabolic panel (BMP; ie, Na, K, Cl, HCO3, BUN, Cr) may be useful in confirming a volume-depleted state. Conversely, a low serum Na level (and sometimes serum Cl) may reflect excessive intravascular free water accumulation. This occurs when a patient receives an HPN formulation that contains a lower concentration of Na than the patient is excreting. Hyponatremia can occur when the patient has a free water excess, such as in patients with liver disease and ascites. In addition, it may be reflective of hypovolemic hyponatremia associated with excessive loss of GI fluids. In patients with normal renal function, hyponatremia is uncommon if the Na concentration of the HPN is in the range of 0.9% NaCl (154 mEq/L). In a stable patient, the development of hyponatremia may take several days to 1 week to develop. Due to free water excess, the Hgb and Hct may decrease in a similar proportion to the decrease in serum Na. Resolution of this problem may be achieved by normalizing the Na delivery in the HPN, by decreasing the free water in the HPN, or by decreasing the high stool or ostomy output. This can be accomplished by using medications such as loperamide or narcotics that can slow GI motility. The clinician should be cautious in using high-Na concentrations in patients who may be prone to congestive heart failure. It is clear that the recognition and management of sodium abnormalities in HPN patients must take into account the full spectrum of a patient's problems rather than reacting to laboratory values alone. Potassium, magnesium, and phosphorus. Potassium (K), magnesium (Mg), and phosphorus (PO4) are intracellular ions that are primarily excreted by the kidney. Potassium is part of a basic metabolic panel (BMP) and the comprehensive metabolic panel (CMP). However, PO4 and Mg are not standard components of a BMP or CMP, so these electrolytes must be ordered separately. Significant losses of K can occur from diarrhea and diuretic use. On initiation of PN, both of these electrolytes can decrease acutely. These changes are primarily due to an intracellular shift in response to anabolism. Generally, HPN is initiated when the patient is in the hospital, and most patients are stable with regard to these electrolytes when discharged home. Although not usually recommended, occasionally a patient starts receiving HPN while in the home. The reader is referred to a recent review for guidelines on initiating PN in the home setting.21 Generally, if renal function is adequate, the K, PO4, and Mg content of HPN can be increased when laboratory values demonstrate that they are below the normal range. Care must be taken, however, to determine the reason for alterations in electrolytes because clinical changes such as increased diarrhea or diuretic use can cause an acute decrease in these levels. An increase in serum concentrations for any of these electrolytes may be due to diminished renal function. Although a change in the HPN formulation is likely, care must be taken to determine the reason for the electrolyte abnormality. If it is determined that a decrease in renal function is the cause, further investigations into the cause of decreasing renal function may be necessary. Calcium. Most of the body's calcium (Ca) resides in the bone. The serum concentration is controlled by a complex endocrine mechanism, with most patients having a Ca that remains in or near the normal range. In addition, total serum Ca concentrations may vary according to serum albumin concentrations. There are several equations available to correct serum Ca concentrations for hypoalbuminemia; however, no specific method has been proven to be accurate. An alternative strategy is to obtain an ionized Ca concentration, which reflects the metabolically active form of Ca. Serum calcium concentrations should be evaluated when other electrolytes are obtained. If the Ca is low, the PN content can be increased, but care must be taken to avoid exceeding an amount that will produce a Ca-PO4 precipitate in the HPN solution. Solubility curves are available to ensure Ca-PO4 limits are not exceeded.
Other Laboratory Values Glucose. Glucose control can be a significant problem in patients receiving HPN. This is due to the large proportion of dextrose calories in the HPN formulation. Patients with tightly controlled serum glucose levels have a lower rate of infections than those who do not.22 However, extrapolating these data to the HPN patient population may not be appropriate because tight glucose control in the home setting has not been adequately studied. Controlling the serum glucose of HPN patients remains challenging but seems intuitively beneficial due to the high risk for infectious complications in this patient population. There are no studies documenting the optimal range of serum glucose concentrations in HPN patients. Despite the lack of evidence, it would seem logical to have glucose control similar to that of other ambulatory patients (ie, <120 mg/dL). Before discharge from a hospital, most HPN patients have their PN cycled (usually over a period of 9–12 hours at night) so they can remain free of HPN for a portion of the day. In addition, there is some evidence that cycling HPN will reduce hepatic complications.23 Blood collection for laboratory parameters is seldom done at night when the patient is asleep; thus, most blood is obtained after the HPN tapers off in the morning. No standard time for obtaining blood samples exists, and the clinician must note the time blood samples are collected in relation to the HPN infusion in order to correctly evaluate the results. For many patients, blood glucose values obtained during cycled HPN infusions do not increase excessively. However, some blood glucoses may be higher than is desired during the HPN infusion. This problem is typically addressed before discharge home receiving HPN. Hyperglycemia can be resolved with addition of insulin to the HPN formulation, altering the cycle time so that HPN is infused over a longer time or reducing the dextrose amount in the HPN formulation. In addition, a longer "ramp-up" time may help reduce the blood glucoses in the initial infusion period. Difficulties in controlling glucose in HPN patients who have been discharged and are at home can also occur. Glucose abnormalities are more frequent in patients with a history of diabetes mellitus, so HPN cycling can be a challenge in this patient population. Evidence of hyperglycemia may be an increased urine output and glucosuria during the HPN infusion. Thus, in patients with marginal to poor glucose tolerance, special care must be taken to measure urine volume, as well as both serum and urine glucoses values, while the HPN is infusing. One potential clue to increased nocturnal urine output is a patient complaint of having to wake frequently at night to urinate. When this occurs in an HPN patient, further investigation may be advisable. Although the cause may be glucosuria, it might also be related to the volume of fluid infused via the HPN.
According to the aforementioned information, careful monitoring of serum
glucose is critical in an HPN patient. It may be desirable to use a glucometer
to monitor glucose, but insurance coverage for these products in nondiabetic
patients may be difficult. A.S.P.E.N. guidelines do not provide a specific
recommendation for serum glucose control in HPN patients. If serum glucose
concentrations are only slightly elevated (ie, 120 mg/dL, with a normal range
of 70–110 mg/dL) and if the blood sample was obtained during the HPN
infusion, this mild elevation is likely not a problem. This is especially true
if the patient has no history of diabetes mellitus and serum glucose
concentrations are in the normal
range3 when HPN is
not infusing. However, significant elevations in serum glucose concentrations
(eg, Low serum glucoses are rare in HPN patients but can occur as rebound hypoglycemia when HPN is tapered off in the morning. Usually, HPN formulations will be tapered over 1 hour by programmable ambulatory pumps. These pumps can be programmed to taper off the HPN in an incremental fashion. Lengthening the "taper-down" time can also assist in reducing the incidence of rebound hypoglycemia. Hypoglycemia can also occur when patients receive insulin (either subcutaneously or in the HPN formulation) and have no oral intake after the infusion is completed.
Lipids. Most long-term HPN patients have IV lipids as a component
of the formulation. Hypertriglyceridemia is one potential complication from
receiving IV lipids on a chronic basis. A.S.P.E.N. guidelines suggest reducing
the lipid dose if the serum triglyceride concentration is
Small-Intestinal Bacterial Overgrowth Consequences of SIBO include an alteration of the enterocyte morphology and function, alteration of nutrient absorption, effects on the immune system, bacteremia due to bacterial migration from the GI tract to the bloodstream, and PN-associated liver disease (PNALD).25–28 In addition, many of these patients develop subtle findings of subjective gastrointestinal discomfort, with symptoms such as excessive flatulence, diarrhea, and abdominal bloating.29 These symptoms are nonspecific, and it is often difficult to determine if the cause is SIBO or is related to other factors such as the patient's underlying disease. Currently, the connection between GI symptoms and bacterial overgrowth are poorly understood for patients with SBS. Management of SIBO includes antibiotic treatment, supplemental prebiotics, or probiotics. There are several anecdotal recommendations on cycling antibiotics and probiotics. Several studies have demonstrated a decrease of bowel bacteria by using antibiotics, but a consistent response in the form of symptom improvement has yet to be demonstrated.30,31
Summary and Conclusions Monitoring for short-term HPN complications requires more than just examining laboratory values. Frequent patient contact (in person or by telephone) is essential to assess the patient. Careful review of all data is the best way to identify, prevent, or manage HPN-associated complications. When devising a plan to address an abnormal laboratory value, it is best to consider the entire patient rather than reacting to an isolated abnormal laboratory value.
Long-term HPN complications can be divided into 2 categories: those that affect organ systems and those that do not. The organ systems that are affected include the liver, kidney, and bones. Of the remainder, some long-term complications are related to nutrient deficiencies or excess. Examples of these are vitamins, fat, and trace metals. Other long-term complications involve issues that are difficult to measure such as quality of life (QOL).
PNALD
Cholestasis may be due to numerous HPN-associated factors, including
sepsis, lipid emulsions, and excessive carbohydrate administration. It is more
commonly observed in the pediatric vs adult population. Laboratory
tests that may be altered include total and conjugated bilirubin, alkaline
phosphatase (ALK PHOS), and sometimes Hepatomegaly and other complications of liver disease such as ascites and encephalopathy may develop in severe cases. When liver damage is significant, diminished liver function can be detected by a reduction in clotting factors. This is reflected by an increase in the international normalized ratio (INR). Some patients dependent on HPN who develop severe hepatic complications may require liver transplantation. The reader is referred to numerous reviews in the literature for more information on this topic.23,35 Nonspecific elevations in ALK PHOS, AST, and/or ALT can occur in patients receiving long-term HPN. The cause of these laboratory abnormalities is not entirely clear. Fatty liver infiltration is often suspected, but a specific association with hepatic histology is not always present.36 As these abnormalities have been associated with the factors listed above, liver function tests should be monitored on a monthly basis. However, less frequent laboratory tests may be appropriate for stable HPN patients. If the laboratory values demonstrate a trend toward significant elevations in bilirubin, ALK PHOS, AST, or ALT (ie, 2–3 times normal), further investigation as to the cause is appropriate. The workup should also evaluate non-HPN-associated causes of liver abnormalities (ie, gallstones, infections, antibiotic use, blood transfusions, hepatitis C).36
Metabolic Bone Disease Although the T and Z scores are considered effective estimates of fracture risk, most patients identified as having a reduced bone mineral density are asymptomatic. Due to the high prevalence of metabolic bone disease and fracture risk in long-term HPN patients, monitoring these patients is important. Numerous causes of HPN-associated metabolic bone disease have been identified, including vitamin D, calcium deficiencies, vitamin K, aluminum, fluoride, copper, silicone, and boron. Corticosteroids have been consistently identified as placing patients at risk for metabolic bone disease. Also, inflammatory bowel disease has been associated with an increased prevalence of metabolic bone disease. The reader is referred to other published reviews for a more detailed discussion of the causes and management of metabolic bone disease in HPN patients.37–40 For evaluation of metabolic bone disease in HPN patients, bone pain, fractures, and DXA results are the major items to monitor. A typical DXA scan measures bone mineral density in several areas, with spine and hip being the most common. A baseline DXA scan should be performed early in a patient whose HPN is likely to be a long-term therapy. Bone mineral density changes appear slowly, so a repeat DXA measurement is not required more frequently than every 12–24 months. It must be noted that many insurance companies will only pay for a DXA measurement every 24 months. If an abnormal bone mineral density measurement is noted to be consistent with osteoporosis, a 24-hour urinary calcium test is recommended. Once the vitamin, calcium, and phosphate content of the HPN is optimized, it is unclear if further modification of the HPN formula will produce a reversal in bone disease. Medications such as bisphosphonates are commonly used and can improve DXA results, but prevention of fracture with these medications in the HPN patient population is controversial.
Parenteral Multivitamins Most of the water-soluble vitamin deficiencies reported in HPN patients have been associated with the B vitamins. Deficiencies in thiamin (vitamin B1) can manifest as anorexia, weight loss, and weakness. Deficiencies in riboflavin can be associated with stomatitis and glossitis. Deficiencies in pyridoxine (vitamin B6) can be associated with dermatitis and a microcytic anemia. Despite the rarity of vitamin deficiencies in HPN patients who properly add parenteral multivitamins to their HPN, adequate monitoring for vitamin deficiencies should be performed in all patients. Routine evaluation of serum blood concentrations for vitamins in HPN patients is recommended on a yearly basis.2 Additional monitoring of vitamin concentrations is appropriate in patients who are suspected of having a vitamin deficiency or excess.
Anemia Unlike iron, cyanocobalamin (vitamin B12) and folate are contained in the multivitamins used in HPN formulations compounded in the U.S. Macrocytic anemia is associated with these 2 vitamins, and the MCV is elevated (often >100 fL). Because the requirement for cyanocobalamin is quite small and parenteral multivitamins used in HPN patients contain an adequate dosage, this deficiency occurs infrequently in HPN patients receiving multivitamins. However, this deficiency can occur in a patient who has inadequate cyanocobalamin absorption and receives HPN only a few times per week. Additional parenteral cyanocobalamin may be required in this rare occasion. Like cyanocobalamin, folate deficiency is quite uncommon in patients receiving HPN with parenteral multivitamins added. However, both folate and cyanocobalamin deficiency must be considered in a patient who has a macrocytic anemia. If folate deficiency is suspected, a serum folate concentration can be obtained. Red blood cell folate is more accurate than serum concentrations, but serum concentrations are more widely available. If folate deficiency is present, additional folate should be added to the HPN formulation.
Trace Elements Zinc deficiencies can occur in patients with high ostomy or stool output accompanied by inadequate replacement.42,43 Symptoms of zinc deficiency can include dry skin or fine rash. Most IV multiple trace element additives provide 2–5 mg of zinc, but this dose may be insufficient if output is high. It is common to obtain zinc concentrations in patients receiving long-term HPN, but the exact correlation of these levels with total body zinc content is not known. If patients develop a low serum zinc concentration or manifest symptoms noted above, it is prudent to increase the zinc provision in the HPN. Supplemental zinc in amounts of 12 mg per mass (kg) of small bowel fluid lost via fistula or 17 mg per mass (kg) of stool or ileostomy output lost may be needed in order to achieve a positive zinc balance.44 Manganese (Mn) is another trace element that is in most multiple trace element solutions. Manganese deficiency is quite rare, but manganese excess in HPN patients has been reported and can be associated with central nervous system abnormalities, including seizures.45 This may be more common in patients who have underlying liver disease as Mn is excreted by the liver. For this reason, we recommend routine monitoring of Mn levels in HPN patients. There are several methods of Mn detection in blood. Although the RBC method may be the more accurate method, there is no evidence that this method is more predictive of toxicity. Even so, the clinician must be aware of the different detection methods as they have different normal ranges. Despite the detection method used, if the concentration is high, removal of Mn provision in the HPN may be indicated. Repeating the Mn concentration after removal from the HPN is also indicated; however, we have demonstrated that an elevated Mn concentration can persist for as long as 1–2 years after removal from the HPN.46 Copper deficiencies have been identified and may result in hematologic abnormalities such as normocytic hypochromic anemia.47 Because copper undergoes hepatic elimination, elevated serum and hepatic copper levels have been identified in patients with underlying liver disease receiving HPN.48 In addition, low copper concentrations have been reported in pediatric patients receiving HPN.49 It is advisable to monitor serum copper on a regular basis, and, if elevated, it should be removed from the HPN. Generally, trace elements are monitored on a yearly basis. Manganese and copper concentrations should be obtained in all HPN patients with underlying liver disease.
Acid-Base Abnormalities
QOL
Patients receiving HPN are often complex patients with many medical problems. In addition to being unable to tolerate adequate oral nutrition, management can be challenging. Clinician input can directly affect the patient's well-being. When monitoring for efficacy, care must be taken to evaluate not only the patient's nutrition response but also the underlying medical problems that are associated with the patient's requirement for HPN. HPN is associated with numerous complications, with a majority of the monitoring directed toward recognition and prevention. Monitoring HPN patients is a complex process involving more than simply ordering and reviewing laboratory values. If the clinician evaluates the whole patient, including laboratory test results and symptoms, there will be a better opportunity to identify and prevent short- and long-term complications associated with HPN.
1 A.S.P.E.N. Board of Directors and the Standards for Specialized
Nutrition Support Task Force; Kovacevich DS, Frederick A, Kelly D, Nishikawa
RA, Young L. Standards for specialized nutrition support: home care patients.
Nutr Clin Pract.2005; 20:579
–590.
Nutrition in Clinical Practice, Vol. 22, No. 3,
340-350 (2007)
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Monitoring: General Concepts
Monitoring for Efficacy
150 mg/dL) should be evaluated promptly. 
glutamyl transferase (GGT).
Although biliary stone formation may occur, biliary sludge has also been
reported. Transaminases such as aspartate aminotransferase (AST) and alanine
aminotransferase (ALT) are abnormal in 40%–50% of patients. Because
these test results are frequently elevated in HPN patients, it is best to use
these laboratory values to screen for liver damage. If abnormal values are
detected, the patient should be completely assessed to determine the cause of
the abnormality. This may include evaluation for alcohol intake and a screen
for viral hepatic disease. When the total bilirubin exceeds 4 mg/dL, scleral
icterus and jaundice may be observed. Specific diagnosis of cholestasis may
require endoscopic retrograde cholangiopancreatography or liver biopsy.