Enteral and Parenteral Nutrition
The ability to provide specialized nutritional support (SNS) represents a major advance in medical therapy. Nutritional support, via either enteral or parenteral routes, is used in two main settings: (1) to provide adequate nutritional intake during the recuperative phase of illness or injury, when the patient's ability to ingest or absorb nutrients is impaired, and (2) to support the patient during the systemic response to inflammation, injury, or infection during an extended critical illness. SNS is also used in patients with permanent loss of intestinal length or function. In addition, an increasing number of elderly patients living in nursing homes and chronic care facilities receive enteral feeding, usually as a consequence of inadequate nutritional intake.
Enteral refers to feeding via a tube placed into the gut to deliver liquid formulas containing all essential nutrients. Parenteral refers to the infusion of complete nutrient solutions into the bloodstream via a peripheral vein or, more commonly, by central venous access to meet nutritional needs. Enteral feeding is generally the preferred route because of benefits derived from maintaining the digestive, absorptive, and immunologic barrier functions of the gastrointestinal tract. Small-bore pliable tubes have largely replaced large-bore rubber tubes, making placement easier and more acceptable to patients. Infusion pumps have also improved the delivery of nutrient solutions.
For short-term use, enteral tubes can be placed via the nose into the stomach, duodenum, or jejunum. For long-term use, these sites can be accessed through the abdominal wall using endoscopic, radiologic, or surgical procedures. Intestinal tolerance of tube feeding may be limited during acute illness by gastric retention or diarrhea. Parenteral feeding has greater risk of infection, reflecting the need for venous access, and a greater propensity for inducing hyperglycemia. However, these risks can generally be managed successfully by SNS teams. For the postoperative patient with preexisting malnutrition, or in trauma patients who were previously well nourished, SNS is strikingly cost-effective. In the most critically ill patient in the intensive care unit, SNS can dramatically enhance survival. Although enteral nutrition (EN) can be provided by most health care teams caring for hospitalized patients, safe and effective parenteral nutrition (PN) usually requires specialized teams.
Approach to the Patient: Requirements for Specialized Nutritional Support
Indications for Specialized Nutritional Support
Although at least 15–20% of patients in acute care hospitals have evidence of significant malnutrition, only a small fraction will benefit from SNS. For others, wasting is an inevitable component of a terminal disease and the course of the disease will not be altered by SNS. The decision to use SNS should be based on the likelihood that preventing protein-calorie malnutrition (PCM) will increase the likelihood of recovery, reduce infection rates, improve healing, or otherwise shorten the hospital stay. In the case of the elderly or chronically ill patient for whom full recovery is not anticipated, the decision to feed is usually based on whether SNS will extend the duration and quality of life. The decision-making process used to decide when to use SNS is depicted in Fig. 73-1.
The first step in deciding to administer SNS is to consider the nutritional implications of the disease process. Is the condition or its treatment likely to impair food intake and absorption for a prolonged period of time? For example, a well-nourished individual can tolerate approximately 7 days of starvation while experiencing a systemic response to inflammation (SRI). The second step is to determine if the patient is already significantly malnourished to the degree that critical functions such as wound healing, immune function, or ventilatory function are impaired. An unintentional weight loss of more than10% during the previous 6 months or a weight/height less than 90% of standard, when associated with physiologic impairment, represents significant PCM. Weight loss less than 20% of usual or less than 80% of standard reflects severe PCM. The presence or absence of SRI should be noted, since inflammation, injury, and infection increase the rate of lean tissue loss. SRI also has pathophysiologic effects that influence nutritional responses such as fluid retention and hyperglycemia, as well as impairment of anabolic responses to nutritional support.
Once it is determined that a patient is already or at risk of becoming malnourished, the next step is to decide whether SNS will impact positively on the patient's response to disease. In the end stages of many chronic illnesses with accompanying PCM, particularly those due to cancer or terminal neurologic disorders, nutrition may not reverse the PCM or improve quality of life. While the provision of food and water is part of basic medical care, nutrition delivered by tube or catheter, either enterally or parenterally, is associated with risk and discomfort. Thus, SNS should be recommended only when potential benefits exceed risks, and should be undertaken with the consent of the patient. Like other life support measures, enteral or parenteral therapy is difficult to withdraw once started. Initiating nutrition support may be appropriate before a final prognosis can be determined, but this should not preclude its subsequent withdrawal. If preventing or treating PCM with SNS is appropriate, nutritional requirements and the method of delivery should be determined. The optimal route depends on the degree of gut function and somewhat on the available technical resources.
The timing of nutritional support is based on evaluation of the preexisting nutritional status, the presence and extent of SRI, and the anticipated clinical course. SRI is identified by the standard clinical signs of leukocytosis, tachycardia, tachypnea, and/or temperature elevation or depression. Although the degree of hypoalbuminemia provides an estimate of SRI severity, normal serum albumin levels will not be restored by adequate nutritional support until the SRI remits, even though nutritional benefits can be achieved by adequate feeding.
The SRI can be graded as severe, moderate, or mild. Examples of severe SRI include sepsis or other inflammatory conditions like pancreatitis requiring ICU care, multiple trauma with an Injury Severity Score more than 20–25 or APACHE II more than 25, closed head injury with a Glasgow Coma Scale less than 8, or major third-degree burns of more than 40% of body surface area. Moderate SRI includes less severe infections, injuries, or inflammatory conditions like pneumonia, major surgery, acute hepatic or renal insufficiency, and exacerbations of ulcerative colitis or regional enteritis requiring hospitalization. PCM should also be defined as severe, moderate, or minimal as assessed by weight/height, percent recent weight loss, and body mass index. The body mass index in relation to nutritional status is listed in Table 73-1. A patient with a severe SRI requires early feeding within the first several days of care because the condition is likely to produce inadequate spontaneous intake over the next 7 days. A moderate SRI, as commonly seen during a postoperative period without oral intake that exceeds 5 days, benefits from adequate feeding by day 5–7 if the patient was initially well nourished. If severely malnourished, candidates for elective major surgery benefit from preoperative nutritional repletion for 5–7 days. However, this is not often possible. Thus, early postoperative feeding is indicated. Patients with a moderate SRI and moderate PCM also benefit from earlier feeding within the first several days.
Table 73-1 Body Mass Index (BMI) and Nutritional Status
More than 30 kg/m2
More than 25–30 kg/m2
Less than 18.5 kg/m2
Less than 16 kg/m2
Less than 13 kg/m2
Less than 11 kg/m2
Lethal in males
Lethal in females
Efficacy of SNS in Different Disease States
Efficacy studies have shown that malnourished patients undergoing major thoracoabdominal surgery benefit from SNS. Critical illness requiring ICU care including major burns, major trauma, severe sepsis, closed head injury, and severe pancreatitis [positive CT scan and Acute Physiology and Chronic Health Evaluation II (APACHE II) more than 10] all benefit by early SNS, as indicated by reduced mortality and morbidity. In critical illness, initiation of SNS within 24 h of injury or ICU admission is associated with a ~50% reduction in mortality. Patients with nitrogen accumulation disorders of renal and hepatic failure have a likelihood of PCM of >50% and at least a moderate SRI. Improvements in morbidity, including infection rates, encephalopathy, liver or renal function, and length of hospital stay have been found with SNS. Inflammatory bowel disease—including Crohn's disease particularly, and, to a lesser degree, ulcerative colitis—often produce PCM. In the outpatient setting, SNS in Crohn's disease can improve nutritional status, quality of life, and the likelihood of remission. With pulmonary disease in the critically ill, SNS improves ventilatory status, and in acute lung injury the use of omega 3 fats as a component of SNS improves gas exchange and respiratory dynamics and reduces the need for mechanical ventilation. Low body weight in chronic obstructive pulmonary disease is associated with diminished pulmonary status and exercise capacity and higher mortality rates. However, there is little convincing evidence that SNS as caloric supplementation improves nutrition or pulmonary function. PCM is also common in the course of cancer and HIV disease, although less so in the latter with the advent of highly active antiretroviral therapy. When PCM develops as a consequence of SRI in these conditions, there is limited likelihood of substantial efficacy or benefit from SNS. However, when PCM develops as a consequence of gastrointestinal dysfunction, SNS can be effective. Although no randomized trials have been performed for SNS provided for hyperemesis gravidarum, there is considerable clinical evidence that it improves pregnancy outcomes.
Risks and Benefits of Specialized Nutrition Support
The risks are determined primarily by patient factors such as state of alertness, swallowing competence, the route of delivery, underlying conditions, and the experience of the supervising clinical team. The safest and least costly approach is to avoid SNS by close attention to oral food intake, by adding an oral liquid supplement, or in certain chronic conditions by using medications to stimulate appetite. Nutrient intake monitoring by frequent calorie counts or oral formula selection is best performed by a nutritionist.
Enteral tube feeding is often required in patients with anorexia, impaired swallowing, or bowel disease. The bowel and its associated digestive organs derive 70% of their required nutrients directly from food in the lumen. Arginine, glutamine, short-chain fatty acids, long-chain omega 3 fatty acids, and nucleotides available in some specialty enteral formulas are particularly important for maintaining immunity. Enteral feeding also supports gut function by stimulating splanchnic blood flow, neuronal activity, IgA antibody release, and secretion of gastrointestinal hormones that stimulate gut trophic activity. These factors support the gut as an immunologic barrier against enteric pathogens. For these reasons, some luminal nutrition should be provided, even when PN is required to provide most of the nutritional support. The combination of some enteral feeding either by mouth or by enteral tube with parenteral feeding often shortens the transition to full enteral feeding, which can generally be used when more than 50% of requirements can be met enterally. Substantial nutritional benefit can be achieved by providing ~50% of energy needs for periods of up to 10 days, if protein and other essential nutrient requirements are met. For longer periods of time, it may be preferable to provide 75–80% of energy needs, rather than full feeding, if this improves gastrointestinal tolerance, glycemic control, and avoidance of excess fluid administration.
In the past, bowel rest through PN was the cornerstone of treatment for many severe gastrointestinal disorders. However, the value of providing even minimal amounts of EN is now widely accepted. The development of protocols to facilitate more widespread use of EN include initiation within 24 h of ICU admission; aggressive use of the head-upright position; postpyloric and nasojejunal feeding tubes; prokinetic agents; more rapid increases in feeding rates; tolerance of higher gastric residuals; and nurse-administered algorithms. PN alone is generally necessary only for severe gut dysfunction due to prolonged ileus, obstruction, or severe hemorrhagic pancreatitis. In the critically ill, feeding adequately by PN beginning within the first 24 h of care improves mortality and is more effective than delayed EN. Early feeding of the critically ill in the ICU is associated with a 50% reduction in mortality, but there is also a 50% increase in infection risk. Much of the increase in morbidity related to PN and EN is due to hyperglycemia, which can be significantly reduced by insulin therapy. The level of glycemia necessary to accomplish this goal, whether less than 110 mg/dL or only less than 150 mg/dL, is not yet defined.
Although PN was initially relatively expensive, its components are often less expensive than specialty enteral formulas. Percutaneous placement of a central venous catheter into the subclavian or internal jugular vein with advancement into the superior vena cava can be accomplished at the bedside by trained personnel using sterile techniques. Peripherally inserted central catheters can also be placed within the lumen in the central vein, but this technique is usually more appropriate for non-ICU patients. The subclavian or internal jugular lines can be changed over a wire, but this carries a greater risk of pneumothorax or serious vascular damage. The peripherally inserted catheters are subject to position-related flow, and the catheter cannot be changed over a wire. Inserting a nasogastric tube is a bedside procedure, but many critically ill patients have impaired gastric emptying that increases the risk of aspiration pneumonia. This risk can be reduced by feeding directly into the jejunum beyond the ligament of Treitz. This usually requires fluoroscopic guidance or endoscopic placement. In patients who have planned laparotomies or other conditions likely to require a prolonged need for SNS, it is advantageous to place a jejunal feeding tube at the time of surgery.
Although most SNS is delivered in hospitals, some patients require it on a long-term basis. If they have a safe environment and a willingness to learn the self-care techniques, SNS can be administered at home. The clinical outcomes of patients with severe intestinal disorders treated with home PN or EN are summarized in Table 73-2. PN infused at home is usually cycled overnight to give greater daytime freedom. Other important considerations in determining the appropriateness of home PN or EN are that the patient's prognosis is longer than several months and that the therapy benefits quality of life.
Disease-Specific Nutritional Support
SNS is basically a support therapy and is primary therapy only for the treatment or prevention of malnutrition. Certain conditions require modification of nutritional support because of organ or system impairment. For instance, in nitrogen accumulation disorders, protein intake may need to be reduced. However, in renal disease, except for brief periods of several days, protein intakes should approach requirement levels of at least 0.8 g/kg or higher up to 1.2 g/kg as long as the blood urea nitrogen does not exceed 100 mg/dL. If this is not possible, then dialysis or hemofiltration should be considered to allow better feeding. In hepatic failure, intakes of 1.2–1.4 g/kg up to the optimal 1.5 g/kg should be attempted, as long as encephalopathy due to protein intolerance is not encountered. In the presence of protein intolerance, formulas containing 33–50% branched-chain amino acids are available at the 1.2–1.4-g/kg level. Cardiac patients, and many severely stressed patients, often benefit from fluid and sodium restriction to levels of 1000 mL of total parenteral nutrition (TPN) formula and 5–20 meq of sodium per day. In patients with severe chronic PCM characterized by severe weight loss and tissue wasting, TPN must be instituted gradually because of the profound antinatriuresis, antidiuresis, and intracellular accumulation of potassium, magnesium, and phosphorus. This is usually accomplished by limiting fluid intakes initially to about 1000 mL containing modest carbohydrate content of 10–20% dextrose, low sodium, and ample potassium, magnesium, and phosphorus, with careful assessment of fluid and electrolyte status. Protein need not be restricted.
The Design of Individual Regimens
The normal daily requirement for fluid is 30 mL/kg of body weight from all sources (IV infusions, per tube, or oral intake), plus any replacement of abnormal losses such as an osmotic diuresis, nasogastric drainage, wound output, or diarrheal/ostomy losses. Electrolyte and mineral losses can be estimated or measured and also need to be replaced (Table 73-3). Fluid restriction may be necessary in patients with fluid overload, and fluid inputs can be limited to 1200 mL/d if urine is the only significant fluid output. When severe fluid overload occurs, the optimal PN solution for central venous administration is a concentrated 1-L solution of 7% crystalline amino acids (70 g) and 21% dextrose (210 g), which provides an amount of nitrogen and glucose that is effective at protein-sparing.
aAll in mEq/L.
Patients requiring PN or EN in the acute care setting generally have some element of associated hormonal adaptations (e.g., increased secretion of antidiuretic hormone, aldosterone, insulin, glucagon, or cortisol) that cause fluid retention and hyperglycemia. Weight gain in the critically ill, whether receiving SNS or not, is invariably the consequence of fluid retention, since lean tissue accretion is minimal in the acute phase of illness. Because excess fluid removal can be difficult, limiting fluid intake to allow for balanced intake and output is more effective.
Total energy expenditure comprises resting energy expenditure (two-thirds) plus activity energy expenditure (one-third). Resting energy expenditure includes the calories necessary for basal metabolism at bed rest. Activity energy expenditure represents one-fourth to one-third of the total, and the thermal effect of feeding is about 10% of the total energy expenditure. For normally nourished healthy individuals, the total energy expenditure is about 30–35 kcal/kg. Although critical illness increases resting energy expenditure, only in initially well-nourished individuals with the highest systemic inflammatory response, such as that from severe multiple trauma, burns, closed head injury, or sepsis, do total energy expenditures reach 40–45 kcal/kg. The chronically ill patient with lean tissue loss has reduced basal energy expenditure, and inactivity which results in a total energy expenditure of about 20–25 kcal/kg. About 95% of such patients need less than 30 kcal/kg to achieve energy balance. Because providing about 50% of measured energy expenditure as SNS is at least equally efficacious for the first 10 days of critical illness, actual measurement of energy expenditure is not generally necessary in the early period of SNS. However, in patients who remain critically ill beyond several weeks, in the severely malnourished for whom estimates of energy expenditure are unreliable, or in those who are difficult to wean from ventilators, it is reasonable to actually measure energy expenditure and to aim for energy balance with SNS.
Insulin resistance is associated with increased gluconeogenesis and reduced glucose utilization, predisposing a patient to hyperglycemia. This is aggravated in patients receiving exogenous carbohydrate from SNS. Normalization of blood glucose levels by insulin infusion in critically ill patients receiving SNS reduces morbidity and mortality. In mild or moderately malnourished patients, a reasonable goal is to provide metabolic support to improve protein synthesis and maintain metabolic homeostasis. Hypocaloric nutrition providing only about 1000 kcal/d and 70 g protein for up to 10 days requires less fluid and reduces the likelihood of poor glycemic control. Energy content can be advanced to 20–25 kcal/kg with 1.5 g protein/kg as conditions permit and definitely during the second week of SNS. Patients with multiple trauma, closed head injury, and severe burns often have much higher energy expenditures, but there is little evidence that providing more than 30 kcal/kg has additional benefit, and it risks hyperglycemia.
Generally, because glucose is an essential tissue fuel, glucose and amino acids are provided parenterally until the level of resting energy expenditure is reached. At this point, adding fat becomes beneficial, since more parenteral glucose stimulates de novo lipogenesis by the liver—an energy-inefficient process. Polyunsaturated long-chain triglycerides are the chief ingredient in most parenteral fat emulsions and the majority of the fat in enteral feeding formulas. These vegetable oil–based emulsions provide essential fatty acids. Enteral feeding formulas have fat content that ranges from 3% of calories up to as much as 50% of calories, while parenteral fat comes in separate containers as 10, 20, and 30% emulsions that can be infused separately or mixed by the pharmacy under controlled conditions as all-in-one or total nutrient admixture with glucose, amino acids, lipid, electrolytes, vitamins, and minerals. Although parenteral fat is required at only about 3% of energy requirements to meet essential fatty acid requirements, when provided as an all-in-one mixture of carbohydrate, fat, and protein, 2–3% fat in the TPN mixtures, representing about 20–30% of calories as fat, is provided to ensure emulsion stability. If given separately, parenteral fat should not be provided at rates exceeding 0.11 g/kg body weight per h or about 100 g over 12 h—equivalent to 1 L of 10% parenteral fat and 500 mL of 20% parenteral fat.
Medium-chain triglycerides, which contain saturated fatty acids with chain lengths of 6, 8, 10, or 12 carbons, are provided in a number of enteral feeding formulas because they are absorbed preferentially. Fish oil contains polyunsaturated fatty acids of the omega 3 family, which have been shown to improve immune function and reduce the inflammatory response. Parenteral emulsions containing medium-chain triglycerides, olive oil, and fish oil are available in Europe and Japan but not yet in the United States.
Carbohydrates are provided as hydrous glucose providing 3.4 kcal/g in PN formulas. In enteral formulas, glucose is the carbohydrate source in so-called monomeric diets. These diets provide protein as amino acids and fat in minimal amounts (3%) to meet essential fatty acid requirements. Monomeric formulas are designed to optimize absorption in the seriously compromised gut. These formulas, like the immune-enhancing diets, are quite expensive. In polymeric diets, the carbohydrate source is usually an osmotically less active polysaccharide, protein is usually soy or casein protein, and fat is present in amounts from 25 to 50%. Such formulas are usually well tolerated by patients with normal intestinal length, and some are acceptable for oral consumption.
Protein or Amino Acid Requirements
Although the recommended dietary allowance for protein is 0.8 g/kg per d, maximal rates of repletion occur with 1.5 g/kg in the malnourished. In the severely catabolic patient, this higher level minimizes protein loss. In patients requiring SNS in the acute care setting, at least 1 g/kg is recommended, with greater amounts up to 1.5 g/kg as volume, renal, and hepatic tolerances allow. The standard parenteral and enteral formulas contain protein of high biologic value and meet the requirements for the eight essential amino acids. In protein-intolerant conditions such as renal and hepatic failure, modified amino acid formulas should be considered. In hepatic failure, higher branched-chain amino acid–enriched formulas appear to improve outcomes. Conditionally essential amino acids like arginine and glutamine may also have some benefit in supplemental amounts.
Protein (nitrogen) balance provides a measure of feeding efficacy of PN or EN. It is calculated as protein intake/6.25 because proteins are on average 16% nitrogen (N), minus the 24-h urine urea N (UUN) plus 4 g N, which reflects other N losses. In the critically ill, a mild negative balance of 2–4 g N/d is usually achievable with a similarly mild positive balance in the recuperating patient. Each g N represents approximately 30 g lean tissue.
Mineral and Vitamin Requirements
Parenteral electrolyte, vitamin, and trace mineral requirements are summarized in Tables 73-4, 73-5, and 73-6. Electrolyte modifications are necessary with substantial gastrointestinal losses from nasogastric drainage or intestinal losses from fistulas, diarrhea or ostomy outputs. Such losses also imply extra calcium, magnesium, and zinc losses. Excessive urine or potassium losses with amphotericin, or magnesium losses with cisplatin or in renal failure, necessitate adjustments in sodium, potassium, magnesium, phosphorus, and acid-base balance. Vitamin and trace element requirements are met by the daily provision of a complete parenteral vitamin supplement and trace elements for PN, and with the provision of adequate amounts of enteral feeding formulas that contain these micronutrients.
aA product is available that does not contain vitamin K. Vitamin K supplementation is recommended at 2–4 mg/week in patients not receiving oral anticoagulation therapy if using this product.
aCommercial products are available that have the first four, first five, and all seven of these metals in recommended amounts.
Infusion Technique and Patient Monitoring
Parenteral feeding through a peripheral vein is limited by osmolality and volume constraints. Solutions that contain more than 3% amino acids and 5% glucose (290 kcal/L) are poorly tolerated peripherally. Parenteral fat (20%) can be given to increase the calories delivered. The total volume required to provide a marginal protein intake of 60 g and 1680 total kcal is 2.5 L. However, the risk of significant morbidity and mortality from incompatibilities of calcium and phosphate salts is greatest in these low-osmolality, low-glucose regimens. Parenteral feeding via a peripheral vein is generally intended as a supplement to oral feeding and is not optimal for the critically ill. Peripheral parenteral nutrition may benefit from small amounts of heparin at 1000 U/L and co-infusion with parenteral fat to reduce osmolality, but volume constraints still limit the value of this therapy. Peripherally inserted central catheters (PICCs) can be used for the short term to provide concentrated glucose parenteral solutions of 20–25% dextrose and 4–7% amino acids, while avoiding some of the complications of catheter placement via a large central vein. With PICC lines, however, flow can be position-related, and the lines cannot be exchanged over a wire for infection monitoring. For these reasons, in the critically ill, centrally placed catheters are preferred. The subclavian approach is best tolerated by the patient and is the easiest to dress. The jugular approach is less likely to lead to a pneumothorax. The femoral approach is discouraged because of the greater risk of catheter infection. For long-term feeding in the home, tunneled catheters and implanted ports reduce infection risk and are more acceptable to patients. However, tunneled catheters require placement in the operating room.
Catheters are made of silastic, polyurethane, or polyvinyl chloride. Silastic catheters are less thrombogenic and are best for tunneled catheters. Polyurethane is best for temporary catheters. Dressing changes with dry gauze at regular intervals should be performed by nurses skilled in catheter care to avoid infection. Chlorhexidine solution is more effective than alcohol or iodine compounds. Appropriate monitoring for patients receiving PN is summarized in Table 73-7.
Note: Hb, hemoglobin; Hct, hematocrit; INR, international normalized ratio; WBC, white blood cell count.
The insertion of a central venous catheter should be performed by trained and experienced personnel using aseptic techniques to limit the major common complications of pneumothorax and inadvertent arterial puncture or injury. Catheter position should be radiographically confirmed to be in the superior vena cava distal to the junction with the jugular or subclavian vein and not directly against the vessel wall. Thrombosis related to the catheter may occur at the site of entry into the vein and extend to encase the catheter. Catheter infection predisposes to thrombosis, as does the systemic inflammatory response. The addition of 6000 U of heparin in the daily parenteral formula in hospitalized patients with temporary catheters reduces the risk of fibrin sheath formation and catheter infection. Temporary catheters that develop a thrombus should be removed and, based on clinical findings, treated with anticoagulants. Thrombolytic therapy can be considered for patients with permanent catheters depending on the ease of replacement and presence of alternate, reasonably acceptable venous access sites. Low-dose warfarin therapy of 1 mg/d reduces the risk of thrombosis in permanent catheters used for home PN, but full anticoagulation may be required in patients who have recurrent thrombosis related to permanent catheters. A recent U.S. Food and Drug Administration mandate to reformulate parenteral multivitamins to include vitamin K at a dose of 150 g daily may affect the efficacy of low-dose warfarin therapy. There is a "no vitamin K" version available for patients receiving this therapy. Catheters can become mechanically occluded and may also become occluded by fibrin at the tip, or by fat, minerals, or drugs intraluminally. These occlusions can be managed with low-dose alteplase for fibrin, with indwelling 70% alcohol for fat, with 0.1 N hydrochloric acid for mineral precipitates, and with either 0.1 N hydrochloric acid or 0.1 N sodium hydroxide for drugs, depending on their pH.
The most common problems related to PN are fluid overload and hyperglycemia (Table 73-8). Hypertonic dextrose stimulates a much higher insulin level than meal feeding. Because insulin is a potent antinatriuretic and antidiuretic hormone, hyperinsulinemia leads to sodium and fluid retention. In the absence of gastrointestinal losses or renal dysfunction, net fluid retention is likely when total fluid intake exceeds 2000 mL/d. Close monitoring of body weight, as well as fluid intake and output, is necessary to prevent this complication. In the absence of significant renal impairment, the sodium content of the urine is likely to be less than 10 meq/L. Providing sodium in limited amounts of 40 meq/d and the use of both glucose and fat in the PN mixture to lower total glucose and sodium will help reduce fluid retention. The elevated insulin also increases the intracellular transport of potassium, magnesium, and phosphorus, which can precipitate a dangerous refeeding syndrome if the total glucose content of the PN solution is advanced too quickly in severely malnourished patients. It is generally best to start PN with less than 200 g glucose/d to assess glucose tolerance. Regular insulin can be added to the PN formula to establish glycemic control, and the insulin doses can be increased proportionately as the glucose is advanced. As a general rule, patients with insulin-dependent diabetes require about twice their usual home insulin doses when they are receiving TPN at 20–25 kcal/kg, largely as a consequence of parenteral glucose administration and some loss of insulin to the TPN container. As a rough estimate, the amount of insulin can be provided in a similar proportion to the amount of calories provided as TPN relative to full feeding, and the insulin can be placed in the TPN formula. Subcutaneous regular insulin can be provided to improve glucose control as assessed by measurements of blood glucose every 6 h. About two-thirds of the total 24-h amount can be added to the next day's order, with subcutaneous insulin supplements as needed. Advances in TPN concentration should be made when reasonable glucose control is established, and the insulin dose adjusted proportionately to the calories added as glucose and amino acids. These are general rules, and they are conservative. Given the adverse clinical impact of hyperglycemia, it may be necessary to use continuous insulin therapy as a separate infusion with a standard protocol to initially establish control. Once established, this insulin dose can be added to the PN formula. Acid-base imbalance is also common during PN therapy. Amino acid formulas are buffered, but critically ill patients are prone to metabolic acidosis, often due to renal tubular impairment. The use of sodium and potassium acetate salts in the PN formula may address this problem. Bicarbonate salts should not be used because they are incompatible with TPN formulations. Nasogastric drainage produces a hypochloremic alkalosis that can be managed by attention to chloride balance. Occasionally, hydrochloric acid may be required for a more rapid response or when diuretic therapy limits the ability to provide substantial sodium chloride. Up to 100 meq/L and up to 150 meq of hydrochloric acid per day may be placed in a fat-free PN formula.
Note: PN, parenteral nutrition.
Infections of the central access catheter rarely occur in the first 72 h. Fever during this period is usually from infection elsewhere or another cause. Fever that develops during PN can be addressed by checking the catheter site and, if the site looks clean, exchanging the catheter over a wire with cultures taken through the catheter and at the catheter tip. If these cultures are negative, as they are most of the time, the new catheter can continue to be used. If a culture is positive for a relatively nonpathogenic bacteria like Staphylococcus epidermidis, consider a second exchange over a wire with repeat cultures or replace the catheter depending on the clinical circumstances. If cultures are positive for more pathogenic bacteria, or for fungi like Candida albicans, it is generally best to replace the catheter at a new site. Whether antibiotic treatment is required is a clinical decision, but C. albicans grown from the blood culture in a patient receiving PN should always be treated because the consequences of failure to treat can be dire.
Catheter infections can be minimized by dedicating the feeding catheter to PN, without blood sampling or medication administration. Central catheter infections are a serious complication with an attributed mortality of 12–25%. Infections in central venous catheters dedicated to feeding should occur less frequently than 3 per 1000 catheter-days. Home PN catheters that become infected may be treated through the catheter without removal of the catheter, particularly if the offending organism is S. epidermidis. Clearing of the biofilm and fibrin sheath by local treatment of the catheter with indwelling alteplase may increase the likelihood of eradication. Antibiotic lock therapy with high concentrations of antibiotic, with or without heparin in addition to systemic therapy, may improve efficacy. Sepsis with hypotension should precipitate catheter removal in either the temporary or permanent PN setting.
Tube Placement and Patient Monitoring
The types of enteral feeding tubes, methods of insertion, their clinical uses, and potential complications are outlined in Table 73-9. The different types of enteral formulas are listed in Table 73-10. Patients receiving EN are at risk for many of the same metabolic complications as those who receive PN and should be monitored in the same manner. EN can be a source of similar problems, but not to the same degree, because the insulin response to EN is about half of that seen with PN. Enteral feeding formulas have fixed electrolyte compositions that are generally modest in sodium and somewhat higher in potassium content. Acid-base disturbances can be addressed to a more limited extent with EN. Acetate salts can be added to the formula to treat chronic metabolic acidosis. Calcium chloride can be added to treat mild chronic metabolic alkalosis. Medications and other additives to enteral feeding formulas can clog the tubes (e.g., calcium chloride may interact with casein-based formulas to produce insoluble calcium caseinate products) and may reduce the efficacy of some drugs (e.g., phenytoin). Since small-bore tubes are easily displaced, tube position should be checked at intervals by aspirating and measuring the pH of the gut fluid (less than 4 in the stomach, more than 6 in the jejunum).
Note: All small tubes are at risk for clogging, especially if used for crushed medications. In long-term enteral patients, gastrostomy and jejunostomy tubes can be exchanged for a low-profile "button" once the tract is established.
Cost: + inexpensive; ++ moderately expensive; +++ very expensive.
The debilitated patient with poor gastric emptying and impairment of swallowing and cough is at risk for aspiration; this is particularly true for those who are mechanically ventilated. Tracheal suctioning induces coughing and gastric regurgitation, and cuffs on endotracheal or tracheostomy tubes seldom protect against aspiration. Preventive measures include elevating the head of the bed to 30 degrees, using nurse-directed algorithms for formula advancement, combining enteral with parenteral feeding, and using post–ligament of Treitz feeding. Tube feeding should not be discontinued for gastric residuals of less than 300 mL unless there are other signs of gastrointestinal intolerance such as nausea, vomiting, or abdominal distention. Continuous feeding using pumps is better tolerated intragastrically and is essential for feeding into the jejunum. For small-bowel feeding, residuals are not assessed but abdominal pain and distention should be monitored.
Enteral feeding often leads to diarrhea, especially if bowel function is compromised by disease or drugs, particularly broad-spectrum antibiotics. Diarrhea may be controlled by the use of a continuous drip, with a fiber-containing formula, or by adding an antidiarrheal agent to the formula. However, Clostridium difficile, which is a common cause of diarrhea in patients being tube fed, should be ruled out before using antidiarrheal agents. H2 blockers may also assist in reducing the net fluid presented to the colon. Diarrhea associated with enteral feeding does not necessarily imply inadequate absorption of nutrients other than water and electrolytes. Amino acids and glucose are particularly well absorbed in the upper small bowel except in the most diseased or shortest bowel. Since luminal nutrients exert trophic effects on the gut mucosa, it is often appropriate to persist with tube feeding, despite the diarrhea, even when this necessitates supplemental parenteral fluid support.