Why would a patient need parenteral nutrition?

Parenteral Nutrition

Parenteral nutrition support includes administration of standard complete nutrient mixtures, which contain dextrose, L-amino acids, lipid emulsion, electrolytes, vitamins, and minerals (and certain medications as indicated, such as insulin or octreotide) given via either a peripheral or central vein. Parenteral nutrition technically also includes parenteral administration of specific micronutrients or micronutrient combinations to replete a deficiency (e.g., thiamine, copper, electrolytes). Administration of complete parenteral nutrition therapy in patients with GI tract dysfunction has become a standard of care in most hospitals and intensive care units throughout the world, although use in individual institutions varies widely. Parenteral nutrition is lifesaving in patients with intestinal failure (e.g., short bowel syndrome); unfortunately, in patient subgroups with lesser degrees of intestinal failure, few objective data from properly designed, large, randomized, controlled studies are available to determine the true efficacy of and optimal indications for parenteral nutrition.A5 Enteral nutrition is at least as good as parenteral nutrition or a combination of the two approaches in patients who can tolerate the former.A6,A7,A7b In patients who cannot tolerate enteral nutrition, early parenteral nutrition is no better than delaying for 3 to 4 days.A8

As a result, the basic principle in considering parenteral nutrition therapy is that the patient must be unable to achieve adequate nutrient intake via the enteral route.9 Compared with parenteral nutrition, enteral nutrition is less expensive, probably maintains intestinal mucosal structure and function to a greater extent, is safer in terms of mechanical and metabolic complications (see below), and is associated with reduced rates of nosocomial infections. Thus, the enteral route of feeding should be utilized and advanced whenever possible and the amount of administered parenteral nutrition correspondingly reduced. Generally recognized indications for parenteral nutrition include:

Patients with short bowel syndrome or other conditions causing intestinal failure which prohibit adequate intake or absorption of enteral nutrients (e.g., motility disorders, obstruction, severe ileus, severe inflammatory bowel disease), especially in those with preexisting malnutrition;

Clinically stable patients in whom adequate enteral feeding (e.g., >50% of needs) is unlikely for 7 to 10 days due to any underlying illness(s);

Patients with severe catabolic stress requiring ICU care in whom adequate enteral nutrient intake is unlikely for more than 3 to 5 days.

Abstract

Parenteral nutrition (PN) is part of specialized nutritional therapy during which nutrients are supplied through the venous system. PN is indicated for the nutritional support of patients who cannot eat, should not eat, or may not be sufficiently fed by oral or enteral routes. Planning for PN and its utilization must be performed by qualified multidisciplinary teams of professionals in order to reduce costs, improve outcomes, and achieve optimal nutrition. Clinical and biochemical markers should be closely monitored to avoid potential PN-related complications. PN should generally be considered as a temporary, supportive mode of nutrition that should be discontinued as soon as conditions for successful oral or enteral diet tolerance are achieved.

Parenteral Nutrition Formulation

To create a PN formula, one must first determine the caloric and protein needs of the patient, which are based on a prior nutritional assessment (seeChapter 5).160 Protein and calorie needs increase with increasing metabolic stress, except in the critically ill. Each component of PN has a defined caloric content, with protein = 4 kcal/g, carbohydrate (dextrose) = 3.4 kcal/g, and IVFE = 10 kcal/g (9 kcal/g from fat, 1 kcal/g from emulsifier). Protein needs vary in the range of 1.2 to 2.0 g/kg/day depending on the level of metabolic stress. Protein should not be restricted, even in patients with severe hepatic encephalopathy or renal failure with azotemia requiring imminent dialysis. Fat is usually provided at 1 g/kg/day, but may need to be reduced or restricted for patients with hypertriglyceridemia (>400 mg/dL). Despite fat restriction, a minimal amount of fat is still given, usually 10% of estimated fat calories (or 500 mL of 20% Intralipid per week), to prevent essential fatty acid deficiency. The remainder of a patient’s daily energy requirements is administered in the form of dextrose. To prevent hyperglycemia and refeeding syndrome (see later under Metabolic Complications), the amount of dextrose should initially not exceed 200 g. Dextrose should be titrated over the course of several days to the goal amount. Water is added to meet the patient’s daily volume needs, with fluid volume restricted in patients with fluid overload, cardiopulmonary disease, or renal failure. Overall water requirements are estimated at 25 to 35 mL/kg/day.

Once the macronutrient components of a PN formula have been defined, electrolytes, trace elements, multivitamins, and medications like insulin, heparin, and PPIs or H2Bs can be added. Any of the components can be increased or decreased based on a patient’s laboratory values and comorbid disease processes. For patients in an unmonitored non-ICU setting, potassium in the PN formula should not exceed 10 mEq/hr. The amount of calcium and phosphorus in the PN solution must also be monitored, owing to the risk of precipitation of calcium-phosphate crystals. In general, the calcium-phosphorus sum ([mEq of calcium + mmol of phosphorus]/L) should be less than 45 to prevent precipitation. Vitamins and trace elements are added using preset solutions, but additional supplementation can be added based on documented needs. Because copper and manganese are excreted in bile, these minerals should be withheld in patients with cholestasis. Selenium should be decreased in patients with renal insufficiency, whereas zinc should be increased in patients with diarrhea, high output fistulas, or large wounds.161 Moderate glycemic control is recommended, keeping serum glucose levels between 110 and 150 mg/dL by sliding scale coverage or addition of insulin to the solution.61 A sample stepwise approach to writing a central PN order is shown inBox 6.1.

Conclusions

Parenteral nutrition as a way to provide essential nutrients is a potentially lifesaving therapy for individuals who are unable to utilize their gastrointestinal tract for a prolonged period of time. Although significant complications may result from this form of therapy, if patients are chosen appropriately and simple precautions such as sterile techniques and close attention to components of the parenteral formulation are taken, these patients would benefit greatly. Management of parenteral nutrition is most effective when done through a multidisciplinary approach, utilizing the expertise of physicians, pharmacists, dieticians, nurses, case managers, and social workers.

Complications of Parenteral Nutrition

Although a myriad of complications of older parenteral nutrition solutions have been reported, with the use of current parenteral formulations most of these are now rare. Some of the complications (electrolyte imbalance, hypoglycemia, hyperglycemia, hypocalcemia, hypercalcemia, hypophosphatemia) can be prevented or corrected by manipulating the constituents of the infusate. The primary complications of parenteral nutrition as currently used are cholestasis and complications related to central lines.

Hepatic dysfunction has long been recognized as an important complication of parenteral nutrition, manifested primarily as cholestatic jaundice. The initial lesion seen histologically is both intracellular and intracanalicular cholestasis, followed by portal inflammation and progressing to bile duct proliferation after several weeks of parenteral nutrition. With prolonged administration, portal fibrosis and ultimately cirrhosis may develop.

The etiology of Parenteral Nutrition Associated Liver Disease (PNALD) is unknown and most likely multifactorial. The patients at greatest risk are critically ill premature infants who are susceptible to multiple insults, such as hypoxia, hemodynamic instability, and sepsis. The most frequently identified risk factors in parenteral nutrition–associated cholestasis are duration of parenteral nutrition, degree of immaturity, and delayed enteral feeding.89 There is expanding evidence that even small-volume enteral feedings can reduce the incidence of cholestasis. Early studies of parenteral nutrition suggested a possible relationship between the quantity of amino acids and hepatic dysfunction. The specific role of the quantity and composition of parenteral amino acids in the cause of cholestatic jaundice in premature infants remains unclear. Some investigators have hypothesized that fish-oil lipid emulsions prevent steatosis, potentially through improved triglyceride clearance and anti-inflammatory properties.4

There have been several case reports in infants of improvement in PNALD with Omegaven.16,26 Using historical controls as a comparison group, Gura and colleagues reported the safety and efficacy of fish oil–based lipid emulsions in 18 infants with short bowel syndrome who developed cholestasis while receiving soybean emulsions.39 At the present time, this therapy is available in the United States only through compassionate-use protocols. Data from randomized clinical trials are needed before recommending a change in clinical practice to include Omegaven for the treatment of PNALD.

Indwelling venous catheters used to deliver PN also may be the source of complications. Both peripheral and central venous routes have been used to deliver PN, but central delivery allows use of more concentrated formulations. Quality initiatives have dramatically reduced the incidence of central line–associated bloodstream infections. In addition, intense nutrition initiatives have reduced the need for prolonged central lines.

Abstract

Parenteral nutrition (PN) is the intravenous administration of nutrients necessary for the maintenance of life. The nutrient components of PN include dextrose, amino acids, fat, electrolytes, multivitamins, and trace elements. Clinicians who are caring for infants and children should pay close attention to the changing nutrient requirements with age, specialized needs of children, vascular access, and the sometimes-limited ability of infants, children, and the critically ill to handle large amounts of fluid, protein, fat, and carbohydrates.1 In the 1960s, Dudrick et al. showed that beagle puppies and, subsequently, an infant could be successfully nourished with the use of PN solutions and central venous access. Since that time, research has promoted substantial advancement in the fields of intravenous access and PN solution components, as well as an improved understanding of the needs of patients with various illnesses to provide individualized care across the spectrum of life. Normal growth and development have been shown in patients exclusively fed by PN.

Indications for Parenteral Nutrition

Parenteral nutrition is indicated when a patient's gastrointestinal tract is either unavailable for use or unreliable for more than 5 to 7 days or when extended bowel rest is desired for therapeutic reasons. Specific indications and contraindications are listed in Box 14-1.

Because there are no situations in which a person should absolutely not be fed, the contraindications are all relative. Surprisingly, some clinicians still tend to resort to TPN when enteral feeding can be used; this should be strongly discouraged. An aggressive commitment to obtaining access for enteral feeding often makes it possible to avoid using TPN.

As in any therapeutic feeding situation, before parenteral nutrition is begun, definitive objectives must be set. The patient's energy and protein requirements should be estimated or measured as described in Chapter 11, and a goal for weight maintenance or weight gain should be clear.

Route of Administration

Parenteral nutrition can be administered via a central or peripheral venous route depending on the available access and the composition of the PN solution. Peripheral PN is generally used for patients whose anticipated period of inadequate enteral feedings is less than 1 week and who have normal fluid requirements.4 It is often difficult to maintain peripheral access for longer than 1 to 2 weeks or to deliver adequate calories with solutions containing 10% or 12.5% dextrose. When hyperosmolar solutions with dextrose concentrations higher than 12.5% are administered through a peripheral intravenous line, there is a risk of phlebitis and thrombosis. Though institution dependent, limiting the infusion of a peripheral solution to a maximum osmolarity of 850 to 1000 mmol is a typical standard of practice.5 Solutions with high dextrose (more than 12.5% dextrose) and calcium concentrations may have increased risk for phlebitis. The concomitant administration of intravenous fat may help decrease phlebitis in a peripheral vein. Depending on the size of the vein, it may not be possible to infuse large volumes or run PN at a high rate.

The central venous route is used for the administration of large fluid volumes at high infusion rates, for hypertonic solutions, and for prolonged administration of PN solutions more than 4 to 6 weeks.5,6 PN may be administered via a peripherally inserted central catheter (PICC), a tunneled central venous catheter (CVC, e.g., Broviac), or an implantable port (e.g., Port-a-Cath). It is recommended the tip of the catheter be placed at the junction of the superior vena cava and right atrium. The best place for a line associated with the least amount of complications is the right internal jugular vein with the tip of the catheter high in the superior vena cava.5,6 This position, corresponding to the level of thoracic vertebra level-T6, is at the level of the right mainstem bronchus and the junction of the right atrium and superior vena cava. When femoral lines or umbilical venous catheters are used, the tip of the catheter should be placed above the level of the diaphragm in the inferior vena cava. Though these two specific catheters are adequate for central infusion, both have increased risk of infection due to the contamination at the exit site.5 Malpositioned catheters, such as those at the level of the renal vessels and those in the liver, should not be used for PN administration because of the risk of thrombosis. It is not recommended that PN be administered via umbilical arterial catheters because of the risk of sepsis. The incidence of peripheral venous access and thrombosis has been well described.7 Measures to prevent thrombosis of vessels include making sure the vessel is not traumatized during insertion of the catheter, using correct tip placement, avoiding the subclavian and femoral veins, always using the smallest catheter possible, using the smallest vein possible, and using an appropriately sized catheter for the vein.8 Other measures utilized to prevent thrombosis include administering PN into a larger vessel, using ultrasound guidance at the time of insertion, removing the CVC as soon as possible, treating CVC blockages early, preventing and treating all infections and venous occlusions, reusing previous access sites for CVC placement, and not placing the CVC into a fibrin sheath. In a patient with poor access, the following sites for placing a CVC may need to be considered: translumbar inferior vena cava, recannulation of the central vein, transhepatic intravenous catheter, use of collateral veins, azygous and hemi-azygous veins, intercostal veins, and putting the line directly into the right atrium. Long lines or PICC lines are threaded into the heart through a large peripheral vein like the antecubital fossa. The success of placement is dependent on the patency of the vein chosen, the presence of valves, and the experience of the person placing the line. PICC lines have been used for over 20 years and are now quite popular because there are few limitations regarding their use related to age, gender, or diagnosis. There is a low incidence of complications with PICC lines, less than 1% for infection, central vein thrombosis, and catheter malposition, as long as their use is limited to 6 to 8 weeks. In addition, significant cost savings are associated with the use of this type of catheter. Contraindications to the placement of PICC lines include dermatitis, cellulitis, burns at or near the insertion site, and previous ipsilateral venous thrombosis.

Patients receiving chronic PN benefit from the placement of a permanent CVC or tunneled silicone elastomer (Silastic) catheter (e.g., Broviac, Hickman and Groshong) and subcutaneous portacaths.9-11 A surgeon or an interventional radiologist using general anesthesia or conscious sedation generally places these catheters. Tunneled catheters can be placed either via a cutdown or percutaneously and have a Dacron cuff located on the midportion of the catheter. This cuff stimulates the formation of dense fibrous adhesions, which anchor the catheter subcutaneously, to prevent dislodgment of the catheter. The cuff also acts as a barrier to bacteria migrating subcutaneously along the catheter surface. Sutures are needed to anchor the catheter at the exit site for several weeks after insertion to allow time for the formation of fibrous adhesions to the Dacron cuff.

Implantable ports are made of plastic or titanium with a compressed silicon disk designed for 1000 to 2000 insertions with a non-coring needle. They are inserted percutaneously into the jugular, subclavian, or cephalic vein and placed in a subcutaneous pocket over the upper chest wall. There are smaller ports available that are primarily used for arm placement and for children. These ports are generally used in situations in which the catheter is only periodically accessed. Patients at high risk for thrombosis of their catheter are those with cancer, those with infections, and those receiving chemotherapeutic agents or PN.

PN can also be delivered via peritoneal or hemodialysis catheters. Intradialytic PN is the administration of PN during dialysis and has been shown to be useful in those patients with end-stage renal disease who do not respond to oral nutritional intervention.12 PN can also be administered to patients who are on extracorporeal membrane oxygenation (ECMO). The dextrose/amino acid solution is administered through the ECMO circuit and intravenous fat is given through a peripheral line to avoid occlusion of the ECMO circuit.13

General information

Parenteral nutrition should be tailored to the needs of the individual, but on average should provide about 25 kcal/kg/day. Solutions for long-term parenteral nutrition should contain:

about 30% carbohydrate, usually in the form of glucose, providing 60% of the energy requirements;

30–50% fat in the form of a lipid emulsion such as soya oil;

amino acids, 150–250 kcal/g of nitrogen;

sodium and potassium;

calcium, phosphate, and magnesium;

bicarbonate;

vitamins;

trace elements (chromium, cobalt, copper, fluoride, iodide, iron, manganese, molybdenum, selenium, zinc).

Parenteral nutrition has been considerably improved by innovative strategies, such as supplementation with medium-chain triglycerides, glutamine, or branch-chain amino acids.

Protein

In parenteral nutrition, nitrogen is administered as amino acids containing all essential and almost all nonessential amino acids. Amino acids are a source of calories and precursors for the biosynthesis of proteins involved in almost every body function. Protein can be oxidized and yields 4 kcal/g. In steady-state conditions, protein oxidation equals protein intake, and under such conditions, exogenous protein serves as an energy supply. However, in Europe, it is generally assumed that in critically ill patients, the structural or biosynthetic function of amino acids outweighs their function as a metabolic fuel. Therefore, parenteral protein in that part of the world is usually not included in the calculation of calorie needs. The dietary reference intake for healthy adults is 0.8 g per kilogram of body weight per day, assuming that total calorie intake is adequate. In patients with more severe disease, such as critically ill patients, 1.2 to 1.5 g/kg may seem more appropriate. Burn patients and patients with important gastrointestinal losses presumably fare better with high-protein regimens (>1.5 g/kg).

The standard formulations for amino acids include solutions containing amino acids only or combinations of amino acids with glucose. Standard amino acid solutions are also available with or without electrolytes. Within the amino acid solutions, different formulations have been tailored to specific disease states. For example, patients with hepatic encephalopathy may benefit from solutions with increased amounts of branched-chain amino acids (valine, leucine, and isoleucine) and reduced amounts of aromatic amino acids. Branched-chain amino acids are oxidized in muscle tissue and therefore may decrease the metabolic burden on the liver. Standard amino acid solutions do not contain glutamine because crystalline l-glutamine is poorly soluble and degrades during heat stabilization. However, glutamine participates intimately in many metabolic processes, including protein synthesis and acid-base balance. Under normal conditions, glutamine is not an essential amino acid, but in critically ill patients, plasma levels fall because endogenous production does not meet increased demand. In critically ill patients, supplemental glutamine in the form of intravenous alanyl-glutamine dipeptide has been shown to improve morbidity and to reduce mortality. However, the interpretation of the available evidence differs, with one guideline recommending the routine use of supplemental glutamine in all patients receiving parenteral nutrition (independent of the concomitant use of enteral nutrition) and another guideline recommending the use only for patients who are exclusively fed with parenteral nutrition.

There is no convincing evidence for specific amino acid compositions in patients with acute renal failure, who may need as much as 1.5 g/kg/day of protein when undergoing renal replacement therapies. This is in contrast to stable patients and those with chronic renal failure, for whom a moderate protein restriction (0.7 to 1.0 g/kg/day) is recommended.