Journal of Parenteral and Enteral

Nutrition http://pen.sagepub.com/

Home Parenteral Nutrition Tutorial

Donald F. Kirby, Mandy L. Corrigan, Rex A. Speerhas and Dorothy M. Emery
JPEN J Parenter Enteral Nutr 2012 36: 632 originally published online 24 September 2012
DOI: 10.1177/0148607112460397

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460397 PENXXX10.1177/014
8607112460397Journal of Parenteral and Enteral Nutrition / Vol. XX, No. X, Month XXXXHome
Parenteral Nutrition Tutorial / Kirby et al
2012

Tutorial

Home Parenteral Nutrition Tutorial Journal of Parenteral and Enteral

Nutrition
Volume 36 Number 6
November 2012 632-644
© 2012 American Society
for Parenteral and Enteral Nutrition
Donald F. Kirby, MD, FACP, FACN, FACG, AGAF, CNSC, CPNS; DOI: 10.1177/0148607112460397
Mandy L. Corrigan, MPH, RD, LD, CNSC; Rex A. Speerhas, RPh, BCNSP; http://jpen.sagepub.com
hosted at
and Dorothy M. Emery, RN http://online.sagepub.com

Abstract
The nutrition support practitioner may be called upon to help coordinate care at home for a patient who requires prolonged intravenous
nutrition after he or she becomes stable enough to leave the hospital. This tutorial reviews the many concepts that must be considered to
manage this type of care successfully. (JPEN J Parenter Enteral Nutr. 2012;36:632-644)

Keywords
home parenteral nutrition; vascular access; adults

Introduction nutrients to sustain themselves. Surgical and medical teams

Dudrick and colleagues1 developed and established the tech-
niques for administering parenteral nutrition (PN) in the
1960s. Since then, home parenteral nutrition (HPN) has come
to be used for patients who require an extension of intravenous
(IV) nutrition beyond the hospital. HPN is not without risk, but
techniques of PN administration in the hospital have been
adapted for use in the home setting. As challenging as it can be
for the patient and additional potential caregivers to administer
this type of therapy at home, it has become much easier with
the availability and evolution of many home care services that
were not available when the first patients went home from our
program in the 1970s. Over the years, infusion devices have
become smaller in size and more portable, thereby reducing
restrictions to allow more freedom of movement so that
patients are not homebound.
Nutrition support teams (NSTs) are commonly composed
of physicians, dietitians, pharmacists, nurses, and social work-
ers, but few hospitals in the United States have home NSTs
managing these complex patients. Proper delivery of HPN
therapy requires an interdisciplinary approach as well as a
clear understanding of the pathophysiology of the underlying
condition, safe solution ordering, fluid and electrolyte manage-
ment, management of short- and long-term infectious and non-
infectious complications, and selection and maintenance of
vascular access devices (VADs). The purpose of this article is
to provide a thorough review of transitioning patients from
hospital to home and management of HPN therapy.
Patient Selection
Patients who have been receiving PN in the hospital
may become stable enough to consider leaving the hospital, but
for a number or reasons, they may not be able to either main-
tain their fluids and electrolytes normally or ingest sufficient
refer patients to NST physicians for determining the appropri-
ateness of HPN therapy in patients with intestinal failure (IF).
IF is defined as a loss of absorptive capacity secondary to
obstruction, dysmotility, surgical resection, congenital defect,
or mucosal disease, resulting in chronic diarrhea, dehydration,
electrolyte abnormalities, micronutrient imbalances, and mal-
nutrition.2 These patients may require HPN for several weeks
or months or indefinitely. Table 1 lists the common etiologies
for HPN. Patients with cancer who cannot maintain fluids and
electrolytes and could be candidates for hospice care will not
be discussed further here.
Table 1. Common Indications for Home Parenteral
Nutrition in Adults
Short bowel syndrome
Radiation enteritis
Severe pancreatitis refractory to enteral nutrition trial
Gastrointestinal motility disorders
High-output gastrointestinal or pancreatic fistulae
Bowel ischemia
Bowel obstruction
Inflammatory bowel disease with malabsorption
Selected oncology patients
From the Cleveland Clinic, Cleveland, Ohio.
Received for publication July 9, 2012; accepted for publication August 10,
2012.
Financial disclosure: none declared
Corresponding Author: Mandy L. Corrigan, MPH, RD, LD, CNSC,
Nutrition Support, Clinician, Home Parenteral Nutrition, Cleveland
Clinic, 9500 Euclid Ave/TT2, Cleveland, OH 44195, USA;
e-mail: corrigm5@ccf.org.

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Home Parenteral Nutrition Tutorial / Kirby et al 633
Table 2. Medicare Criteria for HPN (www.cms.gov)
Massive small bowel resection (leaving ≤5 feet of small bowel
distal to the ligament of Treitz)
Short bowel syndrome (enteral losses exceed 50% of enteral
intake)
Weight loss 10% in ≤3 months
(serum albumin below 3.4 g/dL, fecal fat tests demonstrating malabsorption)
OR
(serum albumin below 3.4 g/dL, gastrointestinal motility disorder refractory to maximum
prokinetic medication, diagnostic test showing dysmotility)
After HPN is deemed necessary, a care plan should be devel-
oped by the interdisciplinary team with patient involvement,
and the patient should understand the risks and benefits of HPN
therapy. The care plan should include the indication for HPN,
the approximate length of HPN therapy, end point (surgery,
spontaneous healing of fistula, resolution of obstruction, transi-
tion to enteral nutrition [EN], etc), and the goals of HPN (weight
gain, weight maintenance, weight loss). After determining the
plan of care, selection of the proper VAD should follow along
with patient education, identification of the HPN caregiver,
insurance review by a nurse case manager, selection of a
homecare agency and infusion pharmacy, evaluation of the
home setting (for safety), and stabilization and cycling of the
HPN solution. For centers providing HPN without management
by a physician lead NST, case managers assist in identifying a
physician to prescribe HPN and coordinating the many differ-
ent skilled therapies that patients may require.
Reimbursement
The case manager or discharge planner plays a critical role in
determining the patient’s insurance benefits and reimburse-
ment for HPN. Costs associated with HPN were estimated at
$140,000 annually in 1992 and are probably higher now.3 For
patients with Medicare, the Centers for Medicare & Medicaid
Services (CMS) criteria must be met for reimbursement of
HPN. Criteria for HPN coverage include the following: HPN
therapy is required for at least 90 days (CMS defines the con-
dition causing the need for HPN therapy to be 90 days or
lifetime as judged to the best of the attending physician’s
knowledge) and weight maintenance cannot be possible using
other methods (enteral feeding or pharmacological interven-
tions). Diagnoses covered by CMS for HPN therapy (see Table
2) include bowel obstruction, pancreatitis, small bowel fistula
(not able to be bypassed with a feeding tube), or intestinal
malabsorption or dysmotility.4 Documentation such as opera-
tive reports, laboratory values, and imaging studies are
required by CMS to support the diagnosis of intestinal failure
requiring HPN. Medicaid benefits and private insurances cov-
erage vary, and benefits should be reviewed by the case man-
ager or discharge planner to ascertain individual benefits.
Patients without insurance coverage provide additional chal-
lenges for the discharge planner. Often, homecare providers
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Complete mechanical small bowel obstruction (inoperable)
Bowel rest for at least 3 months (severe exacerbation of regional
enteritis or proximal enterocutaneous fistula and tube feeding
distal is not possible, symptomatic pancreatitis)
will provide some of the HPN and/or related supplies as char-
ity care, and the patient is required to pay a set cost out of
pocket.
IV Access
One of the most critical decisions that must be made prior to
hospital discharge is how long the intended HPN therapy may
be needed, short vs long term. The answer to this will help in
selecting the most appropriate VAD for each individual
patient. To avoid multiple needless catheterizations, the deci-
sion should be made by collaborating with the primary service,
Infectious Disease Service (if antibiotics are necessary), the
NST physician, and the patient. Advantages/disadvantages for
each VAD include the following: patient/caregiver ability to
care for the VAD, activity level, body image concerns, previ-
ous history of VADs, additional therapies needed, and patient
preference.5 Figure 1 shows the potential sites for IV access.
Choices for vascular access include tunneled VADs with an
anchoring cuff (Hickman/Leonard, Broviac, and Groshong),
implantable ports, and peripherally inserted central catheters
(PICCs). For “short-term” therapy, defined as short to moder-
ate duration (usually weeks), a PICC is often used.6 This can
be placed at the bedside by a specialty team or in interven-
tional radiology. Some advantages of the PICC are the cost-
effectiveness of bedside placement, decreased risk of catheter
insertion complications, and ease of removal upon completion
of HPN therapy. Disadvantages include the following: patient
is less independent with the care of the PICC, dressing must
remain dry, tip migration if the PICC is not secured, and a
greater risk of thrombosis due to the small intraluminal diam-
eter of the catheter.7
For longer term therapy, months to years, tunneled cathe-
ters are the mainstay. Advantages of tunneled catheters are
ease of self-care, they can be used for an extended timeframe,
the cuff aids in the prevention of bacteria migrating into tunnel,
and the ability to repair holes or breaks. However, there is a
lower risk of thrombosis8 with tunneled catheters compared
with PICCs. Implanted ports are another option for long-term
continuous therapy or intermittent therapy. An advantage of a
port is minimal alteration in body image, no concern for acci-
dental pulling or cutting of the device, and patients may go
swimming when the port is not cannulated. A disadvantage is
634 Journal of Parenteral and Enteral Nutrition 36(6)

Figure 1. Common intravenous access sites for home parenteral nutrition.

the needle stick to access the port, and with severe infections,
a surgical procedure is needed for removal.
Another consideration when selecting a VAD is the number
of lumens that will be needed. It is very important for patients
to receive the fewest number of lumens required. Unneeded
lumens require unnecessary manipulation of the catheter,
which increases the chance of infection. Also taken into con-
sideration is the cycle of the HPN solution and if other IV
therapies are required. For instance, with a single lumen, if
antibiotics are ordered every 12 hours, this could be given
before and after the HPN 12-hour cycle. For antibiotics given
more often than every 12 hours, a double lumen would be
required. Selecting the optimal double lumen may help in
decreasing chances of withdrawal or total occlusion complica-
tions (unpublished observation). One option is the Hickman 9
Fr., with the white lumen having the intraluminal size of 0.7
mm and the red lumen 1.3 mm. Another option, the Leonard 10
Fr., is more desirable as both lumens are 1.3 mm. Otherwise,

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Home Parenteral Nutrition Tutorial / Kirby et al 635

Table 3. Central Vascular Access Device Complications

Central Vascular Access Device Complications Symptoms

Exit/insertion site infection Erythema, drainage, swelling, or tenderness
Tunnel infection Pain, swelling, erythema, or induration along the subcutaneous tract of a tunneled
(eg, Hickman or Broviac) catheter
Port pocket infection Tenderness, purulent drainage, and erythema in the subcutaneous pocket of totally
implanted port
Withdrawal/total occlusion Inability to aspirate blood and/or flush the catheter
Pinch-off syndrome Complication of subclavian tunneled central catheter with intermittent/permanent
occlusion related to postural changes
Thrombosis Chest pain; earache; jaw pain; swelling of arm, shoulder, neck, or face on ipsilateral
catheter side; leaking at exit/insertion site
Superior vena cava syndrome Shortness of breath; dyspnea; cough; cyanosis of face neck, shoulder, and arms;
distended chest/neck veins
Air embolus Coughing, shortness of breath, and chest pain
Skin erosion Erythema, skin abrasions, or tears over central venous access device

the Leonard catheter is identical to the Hickman catheter; the
difference between the two is simply the diameter of the
lumens.
Not only is selecting the appropriate VAD of utmost impor-
tance, but also the vessel where the catheter is placed can help
in decreasing possible complications. Figure 1 shows the
potential sites for IV access. The choice of the insertion site is
dependent on many factors such as patient anatomy, chest wall
disease, previous catheters, radiation therapy, implanted defi-
brillator/pacemaker, and previous thrombosis. According to
the Centers for Disease Control and Prevention (CDC), “No
recommendation can be made for a preferred site of insertion
to minimize infection risk for a tunneled central vascular cath-
eter.” However, the CDC does recommend the avoidance of
the femoral site.9
Many preventive strategies and new technologies are avail-
able to help prevent some VAD-related complications (Table
3). Thrombotic catheter occlusion and catheter-related infec-
tions are the most commonly reported catheter complications
for all types of VADs in the healthcare setting. One preventive
strategy to help in decreasing thrombosis is ensuring that the
tip of the VAD is positioned in the right atrium/superior vena
cava (SVC) junction.10 The tip of the catheter should be aligned
with the vessel walls and free floating. According to
Kusminsky,11 malpositioned VADs have been associated with
problems of local toxicity, SVC perforation, and venous
thrombosis. Previously, VADs were placed within the right
atrium, but the current practice opposes this because of the
increased risk of perforation. Other preventive strategies to
help decrease the incidence of thrombotic occlusions and pos-
sible infection would be using proper flushing technique and
correct clamping sequence when disconnecting the syringe
from a needleless connector. It is important to know what type
of fluid displacement the connector has—negative, positive, or
neutral—to prevent blood reflux into the tip of the catheter.12
With negative fluid displacement, disconnecting from the
needleless connector before clamping can cause reflux of
blood back into the catheter. It is recommended when flushing
to leave a small amount of saline in the syringe and while
actively flushing close the clamp. Positive pressure will pre-
vent retrograde of blood into the catheter. With the neutral dis-
placement connector, there is no fluid movement in either
direction when tubing or syringe is disconnected. Flushing
with a positive displacement connector means that when dis-
connecting, a small amount of fluid is forced from the reser-
voir of the connector into the catheter to prevent the reflux of
blood. In this case, clamping after disconnecting is required.
Helping the patient maintain the VAD for the duration of
HPN therapy should be the goal, and measures to help meet
this goal include hand hygiene, access site disinfection, and
providing education to the patient on caring for the VAD.
Solution Basics (Adapted From
Speerhas and Rhoda13)
Components of HPN solutions include protein in the form of
amino acids (AAs), carbohydrate in the form of dextrose, elec-
trolytes, minerals, vitamins, trace elements, medications, and
sterile water for injection. Fat may be added daily to HPN or
administered separately.
Amino Acids
Synthetic crystalline amino acids, which provide 4 kcal/g, are
used in PN as a source of protein. AA solutions are made by a
number of manufacturers, range in concentration from 3%
(30 g/L) to 20% (200 g/L), and are available in standard or
disease-specific formulations.
Standard AA solutions contain 8 essential AAs plus cysteine
and 6 nonessential AAs. Some standard AA solutions (specifi-
cally, FreAmine III [B. Braun, Bethlehem, PA]) also contain an
appreciable amount of phosphate, which must be considered for

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636 Journal of Parenteral and Enteral Nutrition 36(6)

compatibility and when dosing electrolytes. A 10% solution is Table 4. Multivitamin Injection Formulations, 2000
used in PN formulas that do not require concentrated or dis- Ingredient Amount/Unit
ease-specific AAs. Concentrated AA solutions, 15% or 20%,
are available when minimizing fluid intake is required. Fat-soluble vitamins
  A (retinol) 1 mg
Choline is a nonessential AA that is found in many foods,
  D (ergocalciferol or cholecalciferol) 5 mcg
and consequently, deficiencies are rare. Approximately 80% of
  E (α-tocopherol) 10 mg
patients who rely on HPN for their full source of nutrition have
  K (phylloquinone) 150 mcg
been found to have low levels of choline circulating in the
Water-soluble vitamins
blood.14 Some investigators think that choline deficiency may
  C (ascorbic acid) 200 mg
contribute to the development of PN-associated liver disease  B1 (thiamine) 6 mg
(PNALD). Choline is not routinely added to HPN formulas  B2 (riboflavin) 3.6 mg
since it can be synthesized endogenously from methionine and  B6 (pyridoxine) 6 mg
therefore is not an essential AA. In contrast, studies have  B12 (cyanocobalamin) 5 mcg
shown that this pathway may be altered when patients are on   Folic acid 600 mcg
HPN. Buchman et al15 showed that patients receiving HPN  Niacin 40 mg
with choline deficiency and hepatic abnormalities had a rever-   Pantothenic acid 15 mg
sal in these hepatic abnormalities once choline supplementa-  Biotin 60 mcg
tion was started. Further clinical trials are still needed to fully
understand the effect of choline supplementation intravenously
on PNALD, and development of an injectable choline prepara- mL, 20% provides 2 kcal/mL, and 30% provides 3 kcal/mL. A
tion is still needed. minimum of 100 grams of IVFE is required weekly to prevent
EFA deficiency. Other fat emulsions formulations are available
outside the United States but will not be discussed here.
Carbohydrate
Carbohydrate is provided as dextrose and is usually the pri-
mary calorie source in PN. IV dextrose has 3.4 kcal/g and is an
Electrolytes/Minerals
inexpensive, readily available energy source that can be Some electrolytes and minerals are inherent in AA mixtures.
admixed with any AA solution. Commercially available dex- Additional electrolytes and minerals are added to PN in the
trose solutions range in concentration from 5%–70%. amounts based on the individual needs of the patient. Sodium
and potassium are available in salt forms as chloride, acetate,
and phosphate. The gluconate salt of calcium is the preferred
Fat form of this mineral (over calcium chloride) since it is less
Fat is available for IV use as an oil-in-water emulsion. The likely to cause incompatibilities in PN.5 Multichambered PN
emulsified lipid particle ranges from 0.1–0.5 microns in diam- bags are also commercially available with a standard mixture
eter, which is slightly smaller than endogenous chylomicrons. of electrolytes. National shortages of many ingredients con-
All IV fat emulsions (IVFEs) available in the United States tained in PN formulas have occurred, making patient-specific
contain egg phospholipids as an emulsifier, water, and soybean PN very difficult to order.
or safflower oil as a source of polyunsaturated fatty acids.
Glycerol is added to make the emulsion isotonic. Lipid parti-
cles break down and release triglycerides when administered
Vitamins
intravenously. Triglycerides are then hydrolyzed by lipopro- IV vitamin preparations should be added to HPN solutions
tein lipase forming glycerol, free fatty acids, and mono- and daily. Vitamins are commercially available as injectable mul-
diglycerides. The free fatty acids are usually taken up by the tivitamin infusions or single-entity products (with the excep-
tissues and either oxidized for energy or used for resynthesis tion of biotin, pantothenic acid, riboflavin, and vitamins A, D,
of triglycerides and deposition into adipose tissue. and E) (Table 4). There is also an adult multivitamin injection
The primary role of IVFE is to prevent essential fatty acid available without vitamin K. Since this has short-term stability
(EFA) deficiency. Since IVFE contains egg phospholipids, it is in PN solutions, it cannot be compounded by pharmacy for
contraindicated in the (rare) instance of a documented egg HPN, and the patient or caregiver must add this to each PN
allergy. If so, as a last resort, safflower or sunflower oil can be prior to infusion. During times of multivitamin shortages,
administered topically or enterally.16 American Society for Parenteral and Enteral Nutrition
IVFEs containing 10% or 20% fat are isotonic and are the (A.S.P.E.N.) recommends IV vitamin preparations be given 3
source of EFAs when a patient is receiving a dextrose-based times weekly. Chewable vitamin supplements twice daily can
PN solution. The 30% solution is used for compounding total be used for patients with IF on days multivitamin infusion
nutrient admixtures (TNAs). A 10% IVFE provides 1.1 kcal/ (MVI) is not infused.

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Home Parenteral Nutrition Tutorial / Kirby et al 637
Table 5. Adult Multiple Trace Element Injections (Concentration/mL)5
MTE-4 MTE-4 Concentrate
Chromium, mcg 4 10
Copper, mcg 0.4 1 0.4
Manganese, mg 0.1 0.5
Zinc, mg 1 5
Selenium, mcg 0 0
Multiple trace element injections are from American Regent, Inc (Shirley, NY). Single trace element injections are also available for chromium, copper,
manganese, zinc, and selenium.
Table 6. Indications for Adding Histamine-2 Receptor Antagonists to Parenteral Nutrition
Peptic ulcer disease
Gastroesophageal reflux disease (GERD)
Recent extensive small bowel resection with resultant hypergastrinemia
GERD-type symptoms due to ileus or bowel obstruction
Gastrointestinal stress ulcer prophylaxis in high-risk patients (eg, critically ill postoperation)
Trace Elements
Chromium (Cr), copper (Cu), manganese (Mn), selenium (Se),
and zinc (Zn) are the trace elements most commonly added to
HPN. These are commercially available in various combina-
tions or as single-element products (Table 5).
Iron (as iron dextran) may also be added to dextrose-based
PN solutions, but a test dose must first be administered to rule
out an anaphylactic reaction. The addition of iron dextran to
PN solutions should only be considered in cases of docu-
mented iron deficiency anemia when enteral iron supplementa-
tion has failed. Iron cannot be added to a lipid-based PN
formula because it destabilizes the IVFE.17,18 Since iron has
short-term stability in 2-in-1 PN solutions, the patient or care-
giver must add to each lipid-free PN prior to infusion.
Aluminum. Aluminum is a contaminant in all ingredients
used to make PN. Aluminum toxicity has been noted in
patients receiving PN, especially neonates and adults with
renal insufficiency.19
Medications
PN is a complex formulation primarily designed to deliver
nutrients and fluids but can also be used to deliver medica-
tions. Administering medications via HPN is generally not
recommended due to potential drug-nutrient interactions,
compatibility limitations, and the inability to adjust or discon-
tinue the medication without discontinuing HPN. However,
delivering medications via HPN can reduce nursing time and
risk of contamination due to decreased manipulation of IV
lines associated with administering medications separately.
Medications commonly added to HPN are discussed below. A
pharmacist should be consulted before adding any other medi-
cation to HPN.
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MTE-5 MTE-5 Concentrate
4 10
1
0.1 0.5
1 5
20 60
Heparin is not used in HPN patients routinely as it can
cause heparin-induced thrombocytopenia, and if it is used, it
should be withheld in patients actively bleeding.
Regular human insulin is chemically stable in HPN and is
effective in controlling blood glucose when added in appropri-
ate amounts. Insulin should not be routinely added to HPN
unless the patient has a history of diabetes or is demonstrating
glucose intolerance for any reason. Only regular human insulin
should be added to HPN. Insulin has short-term stability in PN
solutions, and the patient or caregiver must add it to each PN
prior to infusion.
Histamine-2 receptor antagonists such as famotidine, raniti-
dine, and cimetidine are used to decrease gastric acid secre-
tions, particularly in patients with massive small bowel
resection or to prevent stress-induced gastropathy. Once added
to HPN, oral and other IV doses of this class of drugs should be
discontinued. The therapeutic dose of famotidine is 40 mg/d.
The dose of these agents must be reduced by half in patients
with renal impairment (creatinine clearance <30 mL/min).
Because histamine-2 receptor antagonists can potentially cause
mental status changes, particularly in the elderly, their use
should be limited to certain conditions. See Table 6 for indica-
tions on adding these agents to PN solutions.
Octreotide is a somatostatin analogue used to decrease gas-
tric, pancreatic, and intestinal secretions; intestinal motility;
and the time needed for gastrointestinal (GI) fistula closure.20
It is also used in graft vs host–induced diarrhea following allo-
geneic bone marrow transplantation.21 The usual starting dose
of octreotide in HPN is 300 mcg/d. There may be a risk of
developing gallstones due to cholestasis (see Table 7).
Octreotide can be safely added to PN solutions, but due to its
short-term stability, it must be added by the patient or care-
giver just prior to infusion of each PN.22 Some pharmacies
may not allow addition of octreotide directly into the PN bag.
638 Journal of Parenteral and Enteral Nutrition 36(6)

Table 7. Suggested Management of Hepatobiliary Abnormalities

Assess ongoing need for PN and ability to start
enteral nutrition
Assess for overfeeding of macronutrients
Assess clinical indication for discontinuation of • Discontinue IV fat emulsion if patient is tolerating adequate amount of fat from
IV lipids
Rule out EFAD
Cycle PN solution
 
Monitor for trace element toxicities
Assess medications or herbal supplements
(promoting cholestasis or hepatotoxicity)
Rule out any infectious causes/sepsis
Assess for bacterial overgrowth
Review medical history for underlying liver
disease and refer to hepatology (for medical
evaluation)
EFAD, essential fatty acid deficiency; IV, intravenous; PN, parenteral nutrition. Source: Corrigan.53 ©2011 Support Line, Dietitians in Nutrition Support,
a dietetic practice group of the Academy of Nutrition and Dietetics. Used with permission.
•  Discontinue/wean PN if able
•  Start enteral nutrition (oral diet, enteral tube feeding)
•  Decrease dextrose or lipid calories if overfeeding present
• Limit IV fat emulsion to lowest dose to prevent EFAD (500 mL of 20% lipid once
weekly) or
• Limit lipid to less than 1 g/kg/d23 if patient requires 3-in-1 PN solutions to achieve
adequate glycemic control (caution needs to be taken to adhere to manufacturing
stability guidelines to ensure a stable 3-in-1 solution)
enteral nutrition47 and does not demonstrate signs of malabsorption
• EFAD is associated with steatosis because of inhibition of fatty acids released
from stored fat in the presence of EFAD26
• Ensure that the patient is not receiving continuous infusion of PN and provide
cycled PN infusion if medically possible48
• Assess for ability to decrease frequently of PN infusion (eg, 6 days per week,
every other day)
• If whole-blood manganese or serum copper values are elevated on laboratory
studies, omit manganese and copper from PN solution49,50
•  Review current medications
• Discontinue antisecretory agents (octreotide) and histamine-2 blockers in PN
solutions that can cause cholestasis51
•  Review any herbal supplements
•  Review for signs of sepsis, including catheter-related sepsis47
• Assess for signs of small bowel bacterial overgrowth in patients with short
bowel syndrome or blind loops and treat with a trial of oral cyclic antibiotics
because released endotoxin reduces bile flow51,52
• Hepatologist referral can initiate necessary diagnostic tests and imaging
(eg, ultrasonography of the right upper quadrant, magnetic resonance
cholangiopancreatography, liver biopsy to describe the full extent and
type of damage) and/or initiate medications (such as ursodiol)

For these patients, octreotide may be injected subcutaneously
or provided as the long acting depot formulation is adminis-
tered every 28 days.
Corticosteroids such as IV methylprednisolone or hydro-
cortisone can be added to HPN for those patients who
need long-term corticosteroid therapy and cannot take oral
corticosteroids. Drawbacks to adding corticosteroids to HPN
solutions include full dose of steroids not being delivered if
there are pump malfunctions or if the HPN solution is
abruptly stopped for any reason. Since steroids have short-
term stability in PN solutions, they cannot be compounded by
the pharmacy for HPN, and the patient or caregiver must add
this to each PN prior to infusion.
Metoclopramide is compatible in PN solutions. Meto-
clopramide is a prokinetic gastrointestinal agent commonly
used for chronic nausea. If chronic IV use is necessary, 20–40
mg/d can be added to PN. However, this is rarely done due to
the high incidence of neurological side effects. Since this has
short-term stability in PN solutions, metoclopramide cannot
be compounded by the pharmacy for HPN, and the patient or
caregiver must add this to each PN prior to infusion.
PN Formula Selection
PN can be compounded as 2-in-1 (dextrose-based) or 3-in-1
(lipid-based) formulations. A 3-in-1, also known as a total
nutrient admixture (TNA), may be administered centrally or
peripherally (home PN therapy does not use the peripheral
route) depending on osmolarity, whereas a 2-in-1 is typically
administered centrally. The patient’s clinical and nutrition
status, estimated duration of therapy, and current IV access
are considerations when determining the type of PN solution.
Osmolarity of PN solutions can be estimated using the for-
mula in Appendix A.
Central PN can be provided as a 2-in-1 solution since there
are no limits on osmolarity when infusing into a central vein.

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Home Parenteral Nutrition Tutorial / Kirby et al 639

The decision to add IV fat emulsions to PN or administer it

separately is based on clinical, physiochemical, and economic
factors.
TNAs may be advantageous when limiting carbohydrate is
warranted due to glucose intolerance. However, IVFEs are
more expensive than dextrose, and adding it to PN creates
issues regarding the stability of the formula and compatibility
with other additives.

Compatibility
Compatibility of a TNA involves the stability of the IVFE.
IVFEs are stable by virtue of a phospholipid coating and
negative electrical charges surrounding each lipid particle,
causing a repellent effect and preventing coalescence. TNAs
have stability problems if improperly compounded (see
Appendix B). Incompatibility can also result from the addition
of inappropriate concentrations of highly positively charged
particles to the TNA. Iron cations, for example, can cause
significant interference with IVFE stability and should not be
added to a TNA. In addition, the total mEq of calcium and
magnesium in a TNA should be restricted (see Appendix B).
If IVFE stability is compromised, creaming or “oiling out”
will occur (see Figure 2). Creaming presents as a skim milk
lower layer with a creamy white layer on the surface of
Figure 2. Cracking or oiling out of intravenous fat emulsion.
the solution. This represents the beginning of emulsion destabi-
lization. At this stage, sufficient shaking will reemulsify the
mixture. “Oiling out” or “cracking” represents a drastic stabil- and trace elements need to be added prior to dispensing from
ity change and is identified when free oil floats on top of the the pharmacy. These commercial solutions of PN are not
TNA solution. When this occurs, the TNA should not be patient specific as they all have the same concentration of
infused. electrolytes or no electrolytes at all. In general, a patient on
The relative solubility of calcium and phosphate is of con- HPN can travel. For short trips, the PN bags can be taken in
cern in all PN solutions. Precipitation of calcium phosphate in cold-storage containers. For longer trips, it is reasonable to ask
PN can occur if the solution is not prepared correctly or the the infusion pharmacy to ship HPN bags and supplies to the
concentrations of calcium and phosphate are too high. If PN is destination. A letter from the prescribing physician may be
compounded with an AA solution containing phosphates necessary for airline travel.
(FreAmine III 10%; B. Braun), this amount of phosphates
should be included in the calculation. See Appendix C for an
equation to calculate calcium and phosphate limits to maintain
Administration
solubility of these components in the PN solution. PN may be cycled or administered continuously. In a hospital
setting, PN is usually infused continuously over a 24-hour
period because it requires less nursing time, effort, and manip-
PN Solution Preparation and Delivery ulation of IV lines. Continuous infusion also generally results
The goal of specialized nutrition support is to provide nutri- in fewer metabolic complications, such as hyperglycemia and
ents in adequate quantities to meet metabolic demands. electrolyte disturbances. PN can be cycled over 8–20 hours to
Individualized PN prescriptions, rather than standard solu- allow time away from the infusion pump when a patient is
tions, are the best way to meet these needs while remaining discharged to an extended-care facility or home. It is recom-
within daily fluid allowances. Standard commercial solutions mended that the PN be cycled and stable (euglycemia) prior to
of PN with or without electrolytes and containing different discharge home from the hospital. One goal is to cycle PN
amino acid and dextrose concentrations are currently avail- over 12 hours each day. This allows the pancreas and liver to
able. These are supplied as dual-chamber bags (none available readapt from the stress of the PN infusion and also provides
in the United States with fat emulsion) and have extended for some enhanced quality of life for the patient. Infusion
stability and a lower aluminum content, and they have poten- pumps can be programmed to taper up 1, 2, or 3 hours and/or
tially less chance of error in compounding as only vitamins taper down 1, 2, or 3 hours to maintain glycemic control

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640 Journal of Parenteral and Enteral Nutrition 36(6)
during and after the PN infusion. Only minor infusion cycle
alterations should be required in the home setting.
Weaning of HPN Solutions
Weaning of HPN solutions differs from weaning hospital PN
solutions. Rather than decreasing the energy or fluid of the
daily solution, calories and fluid are usually reduced by omit-
ting days of the HPN infusion. Once the patient has achieved
his or her goal weight and/or the condition requiring PN ther-
apy has been resolved (ie, malabsorption medically treated,
surgical intervention, etc), typically 7 days of HPN infusions
are reduced to 5 or 6 days if the patient can maintain adequate
hydration. When infusion schedules are changed, laboratory
studies are checked the following week to evaluate fluid and
electrolyte stability. Once intake and output records are
reviewed for fluid balance, weight status is evaluated, and labs
are acceptable, the patient is assessed for ability to wean fur-
ther from PN.
After HPN solutions are reduced to the minimum, 3 days
weekly, the patient’s PN is placed on hold for 1 week. After
laboratory studies are reviewed and found to be normal and the
patient’s weight and enteral intake is assessed to be adequate,
the patient’s VAD is removed and HPN formally discontinued.
Some HPN programs will keep the VAD for several weeks to
months to verify that the patient can be independent of HPN and
does not need to restart and require another invasive catheter
placement, especially if access has been an issue in the past.
HPN Monitoring and Complications
There is a lack of controlled trials with HPN patients and
therefore a lack of evidence-based guidelines for monitoring
and treating potential complications. Long-term complications
may include intes-tinal failure–associated liver disease
(IFALD), metabolic bone disease (MBD), and infectious
(catheter-related bloodstream infections [CRBSIs], site infec-
tions, port-pocket infections, tunnel infections, etc) or nonin-
fectious catheter complications (catheter-related thrombosis,
SVC syndrome, air embolism, occlusions, etc). Other meta-
bolic (fluid and/or electrolyte abnormalities) or mechanical
catheter complications may also occur.
Currently, there are no professional society guidelines for
monitoring HPN patients. Our practice at the Cleveland Clinic
is to obtain labs monthly once the patient is stable. Our lab
monitoring includes a basic metabolic panel, hepatic panel,
phosphorus, magnesium, and complete blood count.
Prealbumin, C-reactive protein, and prothrombin time (PT)/
international normalized ratio (INR) are monitored monthly.
Trace elements (copper, chromium, selenium, zinc, and whole-
blood manganese) are monitored biannually.
Cavicchi et al23 reported the prevalence of liver disease in
HPN patients with permanent IF, noting that 26% of patients
had liver disease after 2 years and 50% after 3 years. The data
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Table 8. Recommendations for Long-term Parenteral
Nutrition Solutions for Prevention and Treatment of
Metabolic Bone Disease
Component Recommendations
Calcium At least 15 mEq/d
Phosphorus Calcium-phosphorus ratio of 1:2 (example: 15
mEq/d calcium and 30 mEq/d phosphorus)
Magnesium Adequate amount to maintain normal serum
magnesium value
Acetate Adequate acetate salts to prevent acidosis and
maintain a normal serum bicarbonate value
Protein 0.8 to 1 g/kg/d protein once stable
Sodium Adequate amount of sodium to maintain normal
serum sodium values, accounting for losses of
sodium via gastric, stool, or urinary routes
Source: Corrigan.53 ©2011 Support Line, Dietitians in Nutrition Support,
a dietetic practice group of the American Dietetic Association. Used with
permission.
clearly show that the incidence of IFALD increased with the
duration of HPN. When liver enzymes suddenly increase or
remain persistently elevated, investigating the cause is war-
ranted (see Table 7 for the suggested management of hepato-
billiary complications). Our institution avoids use of IVFE
daily, but if required based on specific patient comorbidities to
achieve glycemic control, IVFE is be limited to less than 1 g/
kg daily23 (see Table 7).
MBD is used to describe the complex abnormalities of bone
metabolism, density, and strength, such as osteopenia, osteo-
porosis, and osteomalacia.24 Long-term HPN patients are at
risk for developing MBD. MBD is estimated at 84% preva-
lence of osteopenia and 67% prevalence of osteoporosis in
HPN patients.24,25 Patients should be screened for MBD after 1
year of HPN therapy and referred to an endocrinologist if bone
densitometry scan is abnormal. Causes of MBD are poorly
understood. Contributing factors to MBD include medications
and underlying medical conditions, but the contribution of PN
is unknown.26 See Table 8 for HPN solution prevention and
treatment options.
CRBSI is the most common infectious complication of
HPN therapy and is a significant contributor to healthcare
costs, with the average cost of CRBSI ranging from $33,000 to
$65,000 per occurrence.27,28 Tunneled catheters or implanted
ports with the fewest number of lumens necessary should be
used because they have been associated with a decreased inci-
dence of infection.29 The typical presentation of CRBSI
includes fever, rigors, and chills with infusion through the
catheter.30,31 Laboratory findings suggestive of CRBSI can
include positive blood cultures, increased white blood cell
count, and possible elevation of liver enzymes (nonspecific to
CRBSI; elevation may occur with sepsis), but quantitative
blood cultures are the gold standard for diagnosis.
Home Parenteral Nutrition Tutorial / Kirby et al 641
Decreasing HPN Complications
One of the main goals of HPN therapy is to maintain the
patient’s nutrition status while concurrently making all efforts
to minimize complications associated with HPN. CRBSI is
one of the most serious infectious complications of HPN.
Methods to prevent CRBSI have included selecting the VAD
with the fewest number of lumens, institutional hand hygiene
policies, staff and patient training on proper catheter care tech-
niques, maximal barrier precautions during catheter insertion,
aseptic technique during catheter insertion, and removing
catheters no longer in use.9 Instructing the patient on infection
prevention is one of the most critical steps in preventing
catheter-related infections. It is imperative for patients to
receive education on aseptic technique for HPN procedures
and catheter care. Patients should be provided detailed written
instructions, visual demonstration, and the opportunity to repeat
back the procedures. Homecare nursing plays a vital role in
reinforcing the teaching provided to patients while hospitalized
on catheter care, monitoring compliance with procedures, and
monitoring the catheter site. Other techniques have included use
of antibiotic or ethanol lock therapies to prevent CRBSI.
Antibiotic locks have been used to treat CRBSI. Antibiotic
locks consist of 100- to 1000-fold higher concentrations of
antibiotics that dwell within the lumen of the catheter when
cycled HPN is not infusing. Antibiotic locks are used with
systemic antibiotics for treatment of a CRBSI when the goal is
to salvage the VAD. Antibiotic locks should not be used alone
for treatment of CRBSI but in conjunction with systemic anti-
biotics for 7–14 days.32 CDC guidelines9 recommend not
using antibiotic lock for the prevention of CRBSI in general
but can be used prophylactically only in situations with long-
term VADs in patients with a history of multiple cases of
CRBSI. The use of antibiotic locks brings concerns for the
development of resistance or the potential for selection of
worse infectious organisms. The optimal duration of antibi-
otic locks remains unknown.32
Ethanol lock (ETL) has emerged as a method to prevent
CRBSI and has been used in many patient populations, includ-
ing hemodialysis, oncology, and adult and pediatric HPN
patients, but its use is not approved by the Food and Drug
Administration or the Infectious Disease Society of America
due to insufficient data. Benefits of ETL over antibiotic lock
include the following: there is no concern for the development
of resistance (as ethanol acts to denature proteins), it is inexpen-
sive, and it has both bactericidal and fungicidal properties.
Small studies among HPN patients have demonstrated a statis-
tically significant reduction in CRBSI.33-37
Because of the limited number of studies, the optimal dwell
time and strength of ETL are unknown, but it is believed to be
most effective immediately after the central venous access
device (CVAD) is placed, before biofilm has a significant
amount of time to form. Typically, 3 mL of 70% ethanol is
administered after cycled HPN infusions are completed
and allowed to dwell within the lumen of the catheter for the
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longest number of hours the patient is disconnected from HPN.
Before starting the next HPN infusion, ETL is flushed through
the line with normal saline (in adult patients). ETL is com-
monly only used in catheters made from silicone as alcohol has
the potential to act as a solvent with polyurethane materials.
Crinch et al38 examined the mechanical properties of polyure-
thane and silicon catheters after exposure to 70% ethanol for
10 weeks in the lab to investigate the effect on the integrity of
the catheters. The authors report that there was a negligible
impact on the mechanical properties of polyurethane and
silicon catheters and suggest that concerns about the use of
ethanol in these catheter types are less of a concern.
Some literature in the pediatric population shows there may
be increased risk of thrombosis with ETL use, but this has yet
to be documented in the adult population.39,40 More studies are
warranted in this area to define many unanswered questions
regarding the optimal ethanol concentration, optimal dwell
time in the catheter, and studies for cost-savings analysis and if
quality of life is affected in HPN patients. Currently, 70% ETL
locks must be compounded in the pharmacy into a prefilled
syringe. Stability of the compounded ethanol within the
syringe has been studied and documented.41
For patients with hypercoagulable states or those at increased
risk of a catheter-related thrombus, some experts suggest use of
low-dose warfarin (1–2 mg of warfarin/d) to reduce thrombotic
risk prior to insertion of a long-term VAD with continued ther-
apy as long as the VAD is in place. Boraks et al42 demonstrated
decreased incidence of CVAD-related thrombosis in oncology
patients with tunneled catheters given 1 mg/d warfarin upon
insertion until the line was removed. Bern et al43 showed
reduced thrombus related to VAD in oncology patients given 1
mg/d warfarin 3 days prior to VAD placement and continued
therapy for 90 days after placement. Ports were used and cor-
rect placement for the study was defined as within the tip of the
SVC or proximal innominate vein (these lines would currently
be considered malpositioned and at greater risk of thrombus
due to tip location).5,10,44 It is unclear if these results could
transfer to the HPN patient population.
Patients receiving HPN therapy via a VAD may also benefit
from low-dose warfarin therapy; however, past studies within
the PN population have been completed with heparin and not
warfarin. The decision to use this potentially beneficial therapy
in HPN patients is based on clinical judgment of the managing
physician until future studies are completed. Treatment with
anticoagulation prophylaxis in oncology patients receiving
HPN should be strongly considered due to the underlying
increased risk of thrombosis.
Quality of Life
HPN has been a lifeline for patients with intestinal failure
over the years, but quality of life (QOL) can be challenging to
measure. The difficulty in capturing and defining QOL is
determining the impact on QOL from symptoms related to the
primary disease vs the impact from HPN. Tools to measure
642 Journal of Parenteral and Enteral Nutrition 36(6)

Table 9. Intestinal Transplant Criteria4

1. Failure of home parenteral nutrition (HPN)
(a) Impending (total bilirubin above 3–6 mg/dL, progressive thrombocytopenia, and progressive splenomegaly) or overt liver failure
(portal hypertension, hepatosplenomegaly, hepatic fibrosis, or cirrhosis) because of parenteral nutrition liver injury
(b) Central venous catheter (CVC)–related thrombosis of 2 or more central veins
(c) Frequent central line sepsis: 2 or more episodes per year of systemic sepsis secondary to line infections requiring hospitalization,
a single episode of line-related fungemia, septic shock, and/or acute respiratory distress syndrome
(d) Frequent episodes of severe dehydration despite intravenous fluid in addition to HPN
2. High risk of death attributable to the underlying disease
(a) Desmoid tumors associated with familial adenomatous polyposis
(b) Congenital mucosal disorders (ie, microvillus inclusion disease, tufting enteropathy)
(c) Ultra short bowel syndrome (gastrostomy, duodenostomy, residual small bowel <10 cm in infants and <40 cm in older children)
3. Intestinal failure with high morbidity or low acceptance of HPN
(a) Intestinal failure with high morbidity (frequent hospitalization, narcotic dependency) or inability to function (ie, pseudo-
obstruction, high-output stoma)
(b) Patient’s unwillingness to accept long-term HPN (ie, young patients)

QOL that have been validated in the HPN population include
the HPN-QOL, a 48-item questionnaire.45
Due to the need for infusions that last many hours, many
patients talk about the difficulty in getting a good night’s sleep.
Clinicians can offer the patient an option to infuse HPN solu-
tions during the daytime hours to allow for restful sleep during
the night hours. Over the years, equipment such as portable
pumps and backpacks has allowed for enhanced mobility in
the home setting. It is our practice, considering QOL, to assess
the ability to allow patients to infuse HPN solutions 6 nights
weekly if they do not have excessive GI losses or problems
maintaining adequate hydration.
SustainTM
A.S.P.E.N.’s National Patient Registry for Nutrition Care,
called Sustain, has recently been launched. The overall mission
of the prospective, longitudinal registry is to improve patient
outcomes.46 The first phase of registry will help provide infor-
mation on the number of adult and pediatric patients receiving
HPN in the United States, describe patient characteristics and
diagnoses, and evaluate the effectiveness and outcomes of
HPN therapy.46 The eventual goal of Sustain is to include
patients receiving EN. The registry is open to all HPN provid-
ers (physicians or homecare agencies) and is easy to use.
Whether an HPN provider is following 1 or 100 HPN patients,
it is prudent to provide these data to contribute to improving
patient outcomes. For enrollment and additional information on
Sustain, please visit www.nutritioncare.org/sustain.
and networking/peer support for patients receiving home nutri-
tion support therapies. Patients should be made aware of the
Oley Foundation when starting on HPN therapy so they are
aware of the educational, outreach, and networking benefits the
foundation offers. Visit www.oley.org for more information.
Intestinal Transplant Considerations
Despite the general success in managing patients with HPN,
there are instances when patients can and should be considered
for either an isolated small bowel transplant or a multivisceral
transplant. Table 9 lists the current guidelines according to the
CMS. These indications will not be considered further in this
tutorial as intestinal transplant is a separate topic.
Additional Issues
As this detailed discussion has shown, HPN is very labor
intensive and uses many resources. Unfortunately, this man-
agement is either poorly or not reimbursed by insurers and
government agencies alike. This can lead to breaks in manage-
ment and responsibilities that could ultimately affect the
patient. Furthermore, attempts at weaning could create a
“Catch-22” where the patient is under the “minimum reim-
bursable infusion amount,” which could then require the
patient to be responsible for the charges. Insurers and the
government should work with physicians and appropriate
societies to more fairly compensate those for their time and
efforts to keep patients out of the hospital and give them hope
for an improved QOL.

Oley Foundation
The Oley Foundation is a nonprofit, national organization
founded in 1983 that assists patients who receive HPN and
home EN. The Oley Foundation provides a patient-focused
educational newsletter, annual conference (for patients/clinicians),
Conclusion
The provision of HPN requires a coordinated multimodality
approach to provide a costly, high-tech therapy at home.
Although patients can do very well, vigilance to maximize

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Home Parenteral Nutrition Tutorial / Kirby et al 643
QOL and to minimize potential complications takes significant
effort on both the patients’ and clinicians’ behalf to form a
beneficial symbiotic therapeutic partnership.
Appendix A
Calculating the Osmolarity of PN Solutions
A. Total grams of AA per liter of solution ____ × 10 =
____ mOsm
B. Total grams of dextrose per liter of solution ____ × 5
= ____ mOsm
C. Total grams of fat (30% emulsion) per liter of solu-
tion ____ × 0.67 =____ mOsm
D. Total mEq of calcium, magnesium, potassium, and
sodium per liter of solution ____ × 2 =____ mOsm
Add A, B, C, and D to derive the osmolarity of the PN solution
= _____ mOsm/L.
Example: PN solution containing 1800 kcal, 80 g amino
acids, and nonprotein calorie distribution of 70% dextrose and
30% lipid in a 2400-mL volume plus 200 total mEq of calcium,
magnesium, potassium, and phosphorus:
A. 80 g AA/2.4 L = 33 g AA/L × 10 = 333 mOsm
B. 304.7 g dextrose/2.4 L = 127 g dextrose/L × 5 = 635
mOsm
C. 148 g lipid/2.4 L = 61.7 g lipid/L × 0.67 = 41 mOsm
D. 200 mEq lytes/2.4 L = 83 mEq/L × 2 = 167 mOsm
Total osmolarity = 1176 mOsm (must be infused with a
central venous catheter if osmolarity is >900 mOsm)
Appendix B
Compatibility Compounding Guidelines Used
by Cleveland Clinic for 3-in-1 PN Solutions13
PN Component Compatibility Range
Amino acid 20–60 g/L (80–240 kcal/L)
Dextrose 40–250 g/L (138–850 kcal/L)
Lipid 20–60 g/L (200–600 kcal/L)
Divalent cations ≤20 mEq/L
(magnesium and calcium)
Appendix C
Calculating Calcium and Phosphate Solubility13
(Should Not Exceed 200)
mEq Calcium/L × mEq phosphatesa/L  200.
a
Sodium phosphates, potassium phosphates, and FreAmine
10% amino acids (10 mmol per 100 g of AA).
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Appendix D
Glossary
CRBSI Catheter-related bloodstream infection: a sys-
temic infection involving the catheter.
CVAD Central venous access device: a catheter whose
tip optimally lies in the lower third of the superior
vena cava adjacent to the right atrium.
HPN Home parenteral nutrition: the provision of intra-
venous nutrition at home.
PICC Peripherally inserted central catheter: a catheter
inserted peripherally (usually in the basilic, brachial,
or cephalic veins) and advanced centrally into the
superior vena cava.
PN Parenteral nutrition (or central vein nutrition): refers
to nutrition support that is delivered via a catheter tip
that optimally lies in the lower third of the superior
vena cava adjacent to the right atrium. This allows
optimal mixing of highly osmolar solutions due to
turbulent blood flow and decreases the risk of venous
thrombosis related to PN therapy.
References
  1. Dudrick SJ, Wilmore DW, Vars HM, Rhodes JE. Long-term total paren-
teral nutrition with growth, development, and positive nitrogen balance.
Surgery. 1968;64:134-142.
 2. O’Keefe S, Buchman A, Fishbein T, et al. Short bowel syndrome and
intestinal failure: consensus definitions and overview. Clin Gastroenterol
Hepatol. 2006;4:6-10.
  3. Howard L. Home parenteral nutrition: survival, cost, and quality of life.
Gastroenterology. 2006;130:S52-S59.
  4. Center for Medicare and Medicaid Services, U.S. Department of Health
and Human Services. Meeting your Medicare needs. http://apps.ngsmedi-
care.com/applications/Content.aspx?DOCID=20493&CatID=3&RegID=
51&ContentID=34464. Accessed April 2, 2012.
  5. Mirtallo J, Canada T, Johnson D, et al. Safe practices for parenteral nutri-
tion. JPEN J Parenter Enteral Nutr. 2004;28:S39-S70.
  6. Emery M, Stafford J, Pearson A, Steiger E. Venous access and catheter
care. In: Coughlin KL, DeChicco R, Hamilton C, eds. Cleveland Clinic
Nutrition Support Team Manual. Cleveland, OH: Cleveland Clinic; 2011:
121-142.
  7. Paauw JD, Borders H, Ingalls N, et al. The incidence of PICC line-associ-
ated thrombosis with and without the use of prophylactic anticoagulants.
JPEN J Parenter Enteral Nutr. 2008;32:443-447.
  8. Moureau N, Poole S, Murdock MA, et al. Central venous catheters in home
infusion care: outcomes analysis in 50,470 patients. J Vasc Interv Radiol.
2002;13:1009-1016.
  9. O’Grady NP, Alexander M, Burns LA, et al. Guidelines for the preven-
tion of intravascular catheter related infections. Am J Infect Control.
2011;39:S1-S34.
10. Steiger E. Dysfunction and thrombotic complications of vascular access
devices. JPEN J Parenter Enteral Nutr. 2006;30:S70-S72.
11. Kusminsky RE. Complications of central venous catheterization. J Am
Coll Surg. 2007;204:681-696.
644 Journal of Parenteral and Enteral Nutrition 36(6)
12. Hadaway L. Flushing vascular access catheters: risks for infection trans-
mission. Infect Control Resource. 2005;4:1-6.
13. Speerhas R, Rhoda K. Parenteral nutrition. In: Coughlin KL, DeChicco R,
Hamilton C, eds. Cleveland Clinic Nutrition Support Team Manual. Cleve-
land, OH: Cleveland Clinic; 2011:81-98.
14. Chawla RK, Berry CJ, Kutner MH, Rudman D. Plasma concentrations of
transsulfuration pathway products during nasoenteral and intravenous hyper-
alimentation of malnourished patients. Am J Clin Nutr. 1985;42:577-584.
15. Buchman AL, Ament ME, Sohel M, et al. Choline deficiency causes
reversible hepatic abnormalities in patients receiving parenteral nutrition:
proof of a human choline requirement: a placebo controlled trial. JPEN J
Parenter Enteral Nutr. 2001;25;260-268.
16. Miller DG, Williams SK, Palombo JD, Griffin RE, Bistrian BR, Blackburn
GL. Cutaneous application of safflower oil in preventing essential fatty
acid deficiency in patients on home parenteral nutrition. Am J Clin Nutr.
1987;46:419-423.
17. Kalista-Richards M, Cook HC. Iron as an essential micronutrient. Support
Line. 2002;24:17-22.
18. Kumpf VJ. Update on parenteral iron therapy. Nutr Clin Pract. 2003;
18:318-326.
19. Speerhas RA, Seidner DL. Measured versus estimated aluminum content of
parenteral nutrition solutions. Am J Health Syst Pharm. 2007;64:740-746.
20. Torres AJ, Landa JI, Moreno-Azcoita M, et al. Somatostatin in the manage-
ment of gastrointestinal fistulas. Arch Surg. 1992;127:97-99.
21. Ippoliti C, Champlin R, Bugazia N, et al. Use of octreotide in the symptom-
atic management of diarrhea induced by graft-versus-host disease in patients
with hematologic malignancies. J Clin Oncol. 1997;15:3350-3354.
22. Seidner DL, Speerhas RA. Can octreotide be added to parenteral nutrition
solutions? Point-counterpoint. Nutr Clin Pract. 1998;13:84-87.
23. Cavicchi M, Beau P, Crenn P, et al. Prevalence of liver disease and contrib-
uting factors in patients receiving home parenteral nutrition for permanent
intestinal failure. Ann Intern Med. 2000;132:523-532.
24. Cohen-Solal M, Baudoin C, Joly F, et al. Osteoporosis in patients on long-
term home parenteral nutrition: a longitudinal study. J Bone Miner Res.
2003;18:1989-1998.
25. Pironi L, Morselli AM, Pertkiewicz M, et al. Prevalence of bone disease in
patients on home parenteral nutrition. Clin Nutr. 2002;21:289-296.
26. Kumpf V, Gervasio J. Complications of parenteral nutrition. In: Gott-
schlich MM, DeLegge MH, Mattox T, Mueller C, Worthington P, eds. 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; 2007:323-339.
27. Pittet D, Tarara D, Wenzel RP. Nosocomial blood stream infection in criti-
cally ill patients: excess length of stay, extra costs, and attributable mortal-
ity. JAMA. 1994;271:1598-1601.
28. Orsi GB, Di Stefano L, Noah N. Hospital acquired, laboratory confirmed
bloodstream infection: increased hospital stay and direct costs. Infect Con-
trol Hosp Epidemiol. 2002;23:190-197.
29. Tokars JI. Cookson ST, McArthur MA, et al. Prospective evaluation of
risk factors for bloodstream infection in patients receiving home infusion
therapy. Ann Intern Med. 1999;131:340-347.
30. Krzywda EA, Andris DA, Edmiston CE, Wallace JR. Parenteral access
devices. In: Gottschlich MM, DeLegge MH, Mattox T, Mueller C,
Worthington P, eds. 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; 2007:300-322.
31. Fuhrman MP. Complication management in parenteral nutrition. In: Mata-
rese LE, Gottschlich MM, eds. Contemporary Nutrition Support Practice:
A Clinical Guide. 2nd ed. St Louis, MO: Saunders Co; 2003:242-262.
32. Mermel LA, Allon M, Bouza E, et al. Clinical practice guidelines for the
diagnosis and management of intravascular catheter-related infection:
2009 update by the Infectious Diseases Society of America. Clin Infect
Dis. 2009;49:1-45.
Downloaded from pen.sagepub.com by J.luis G. de la Rosa on October 31, 2012
33. Opilla MT, Kirby DF, Edmond MB. Use of ethanol lock therapy to reduce
the incidence of catheter-related bloodstream infections in home parenteral
nutrition patients. JPEN J Parenter Enteral Nutr. 2007;31:302-305.
34. Mouw E, Chessman K, Lesher A, Tagge E. Use of an ethanol lock to pre-
vent catheter-related infections in children with short bowel syndrome. J
Ped Surg. 2008;43:1025-1029.
35. John BK, Khan MA, Speerhas R, et al. Ethanol lock therapy in reducing
catheter-related bloodstream infections in adult home parenteral nutrition
patients: results of a retrospective study. JPEN J Parenter Enteral Nutr.
2012;36(5):603-610.
36. Jones BA, Hull MA, Richardson DS, et al. Efficacy of ethanol locks in
reducing central venous catheter infections in pediatric patients with intes-
tinal failure. J Ped Surg. 2010;45:1287-1293.
37. Metcalf SC, Chambers ST, Pithie AD. Use of ethanol locks to prevent
recurrent central line sepsis. J Infect. 2004;49:20-22.
38. Crinch CJ, Halfmann JA, Crone WC, Maki DG. The effects of prolonged
ethanol exposure on the mechanical properties of polyurethane and silicon
catheters used for intravascular access. Infect Control Hosp Epidemiol.
2005;26:708-714.
39. Wong T, Clifford V, McCallum Z, et al. Central venous catheter thrombosis
associated with 70% ethanol locks in pediatric intestinal failure patients on
home parenteral nutrition: a case series [published online October 5, 2011].
JPEN J Parenter Enteral Nutr. doi:10.1177/0148607111414713.
40. Oliveria C, Nasar A, Brindle M, Wales PW. Ethanol locks to prevent cath-
eter related blood stream infections in parenteral nutrition: a meta-analysis.
Pediatrics. 2002;129:318-329.
41. Cober MP, Johnson CE. Stability of 70% alcohol solutions in polypro-
pylene syringes for use in ethanol-lock therapy. Am J Health Syst Pharm.
2007;64:2480-2482.
42. Boraks P, Seale J, Price J, et al. Prevention of central venous catheter asso-
ciated thrombus using minidose warfarin in patients with haematological
malignancies. Br J Haematol. 1998;101:483-486.
43. Bern MM, Lokich JJ, Wallach SR, et al. Very low doses of warfarin
can prevent thrombosis in central venous catheters. Ann Intern Med.
1990;112;423-428.
44. DeChicco R, Seidner DL, Brun C, Steiger E, Stafford J, Lopez R. Tip posi-
tion of long-term central venous access devices used for parenteral nutri-
tion. JPEN J Parenter Enteral Nutr. 2007;31:382-387.
45. Baxter JP, Fayers PM, McKinley AW. The clinical and psychometric
validation of a questionnaire to assess the quality of life of adult patients
treated with long-term parenteral nutrition. JPEN J Parenter Enteral Nutr.
2010;34:131-142.
46. Guenter P, Robinson L, DiMaria-Ghalili RA, Lyman B, Steiger E, Win-
kler MF. Development of Sustain: A.S.P.E.N.’s national patient registry for
nutrition care. JPEN J Parenter Enteral Nutr. 2012;36(4):399-406.
47. Corrigan ML, John BK, Steiger E. Parenteral nutrition. In: Mullen GE,
Matarese LE, Palmer M, eds. The Gastrointestinal and Liver Disease
Nutrition Desk Reference. Boca Raton, FL: CRC Press; 2011:343-358.
48. Hwang T, Lue M, Chen L. Early use of cyclic TPN prevents further dete-
rioration of liver functions for the TPN patients with impaired liver func-
tion. Hepatogasteroenterology. 2000;47:1347-1350.
49. Jensen GL, Brinkley J. Clinical manifestations of nutrient deficiencies.
JPEN J Parenter Enteral Nutr. 2002;26:S29-S33.
50. Fessler TA. Trace element monitoring and therapy for adult patients receiv-
ing long-term total parenteral nutrition. Pract Gastroenterol. 2005;25:44,
51-52, 54, 56, 58, 60, 63-65.
51. Jeejeehboy KN. Management of PN-induced cholestasis. Pract Gastroen-
terol. 2005;24:62-68.
52. Fuhrman MP. Complication management in parenteral nutrition. In: Mata-
rese LE, Gottschlich MM, eds. Contemporary Nutrition Support Practice:
A Clinical Guide. 2nd ed. St Louis, MO: Saunders Co; 2003:242-262.
53. Corrigan ML. Complications of home parenteral nutrition. Support Line.
2011;33:3-12.