Nutrition Alterations and Management

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Nutrition Alterations and Management

Kasuen Mauldin

Nutrition support is an essential component of providing comprehensive care to the critically ill patient. Nutrition screening must be conducted on every patient, and a more thorough nutrition assessment completed on any patient screened to be nutritionally at risk. Malnutrition can be related to any essential nutrient or nutrients. A serious type of malnutrition found frequently among hospitalized patients is protein-calorie malnutrition (PCM). Malnutrition is associated with a variety of adverse outcomes, such as wound dehiscence, infections, pressure ulcers, respiratory failure requiring ventilation, longer hospital days, and death. The purpose of this chapter is to provide an overview of nutrient metabolism, nutritional status assessment, and implications of undernutrition for the sick or stressed patient. Specifically, nutrition for each of the system alterations will be discussed along with nursing management.

Nutrient Metabolism

Nutrients are chemical substances found in foods that are needed for human life, growth, maintenance, and repair of body tissues. The main nutrients in foods are carbohydrates, proteins, fats, vitamins, minerals, and water. The process by which nutrients are used at the cellular level is known as metabolism. The energy-yielding nutrients or macronutrients are carbohydrates, proteins, and fats. For proper metabolic functioning, adequate amounts of micronutrients, such as vitamins, minerals (including electrolytes), and trace elements also must be supplied to the human body.

Energy-Yielding Nutrients

Carbohydrates

Through the process of digestion, carbohydrates are broken down into glucose, fructose, and galactose. After absorption from the intestinal tract, fructose and galactose are converted to glucose, the primary form of carbohydrate used by the cells. Glucose provides the energy needed to maintain cellular functions, including transport across cell membranes, secretion of specific hormones, muscle contraction, and synthesis of new substances. Most of the energy produced from carbohydrate metabolism is used to form adenosine triphosphate (ATP), the principal form of immediately available energy within all body cells. One gram of carbohydrate provides approximately 4 kcal of energy. For example, if a food contains 10 grams of carbohydrates, then 40 kcal (10 g × 4 kcal/g) of the total calories for that food comes from carbohydrates.

Inside the cell, glucose can be stored as glycogen or metabolized in a process called glycolysis for the subsequent release of energy. Liver and muscle cells have the largest glycogen reserves. In addition to glucose obtained from glycogen, glucose can be formed from lactate, amino acids, and glycerol. This process of manufacturing glucose from non-glucose precursors is called gluconeogenesis. Gluconeogenesis is carried out at all times, but it becomes especially important in maintaining a source of glucose in times of increased physiologic need and limited supply. Only the liver and, to a lesser extent, the kidney are capable of producing significant amounts of glucose for release into the blood for use by other tissues.

Proteins

Proteins are made up of chains of amino acids. Each amino acid consists of carbon, hydrogen, and oxygen, and nitrogen in the form of one or more amine groups (imageNH2). Amino acids are the protein components that can be used by cells.

Proteins have important structural and functional duties within the body. Proteins provide the structural basis of all lean body mass, such as the vital organs and skeletal muscle. Proteins are important for visceral (cellular) functions, such as initiation of chemical reactions (e.g., hormones, enzymes), transportation of other substances (e.g., apoproteins, albumin), preservation of immune function (e.g., antibodies), and maintenance of osmotic pressure (e.g., albumin) and blood neutrality (e.g., buffers). Some amino acids are used for energy, providing approximately 4 kcal per gram.

Proteins are synthesized continuously, broken down into amino acids, and then resynthesized into new protein. This three-step process is called protein turnover. The rate of turnover is fastest (often only a few hours) in enzymes and hormones involved in metabolic activities. In very active tissues—such as those of the liver, kidney, and gastrointestinal mucosa—protein turnover occurs every few days. If necessary, 90% of the amino acids released by tissue breakdown can be reused, with the diet providing the remaining 10% of the amino acids needed for protein synthesis. In the injured or undernourished individual, many of the amino acids released by tissue breakdown may be used for gluconeogenesis. To preserve lean body mass, adequate energy must be supplied by the diet so that most of the amino acids from the diet and from tissue breakdown can be used for tissue synthesis, rather than gluconeogenesis.

Proteins, which often consist of hundreds or thousands of amino acids, are too large to be absorbed intact under normal circumstances. Through digestion, the proteins are broken down into amino acids and dipeptides or tripeptides (composed of two or three amino acids, respectively) that can be absorbed across the intestinal wall. Certain amino acids are essential; they cannot be produced by the body and must be supplied through the diet. Essential amino acids include valine, leucine, isoleucine, lysine, phenylalanine, tryptophan, threonine, and methionine, as well as histidine and arginine in infants. Other amino acids are nonessential and can be manufactured by the body under normal circumstances if the essential amino acids are in adequate supply. Some amino acids that may be nonessential in healthy adults become essential during illness. For example, histidine is an essential amino acid for adults with renal failure, and glutamine may be essential for individuals with trauma, sepsis, or other physiologic types of stress.

The amine group is essential for protein synthesis, but the nonamine portion of the molecule (ketoacid) is used in gluconeogenesis. If a ketoacid is used for gluconeogenesis, the amine group can be excreted in the urine as ammonia or urea. If the rate of gluconeogenesis rises, urinary nitrogen excretion also increases. In assessing protein nutrition, it is common to measure nitrogen balance, or the amount of nitrogen excreted compared with that consumed. Normally, most of the body’s nitrogen losses are in the urine, and in determining nitrogen balance, urinary nitrogen excretion is measured (preferably over a 24-hour period). Nitrogen (protein) intake is recorded over the same period, and losses of nitrogen from feces and other routes (e.g., sloughing of skin cells) are usually estimated.

Most healthy adults are in nitrogen equilibrium, meaning that they excrete the same amount of nitrogen that they consume. Individuals who excrete less nitrogen than they consume are said to be in positive nitrogen balance; this occurs during growth, pregnancy, and healing. Individuals who excrete more nitrogen than they consume are in negative nitrogen balance. Negative nitrogen balance is common in the early period after trauma or surgery. When the rate of gluconeogenesis is high, as may occur in the trauma patient who is initially too unstable to be fed, extensive loss of body proteins can occur. Losses include structural (e.g., muscle) and visceral proteins. Visceral proteins, including immunoglobulins, albumin, and complement, are critical for survival. Preservation of body protein is therefore a key goal of nutrition support of critically ill patients.

Lipids (Fats)

Lipids include fatty acids, triglycerides (three fatty acids bound to a glycerol backbone), phospholipids (lipids containing phosphate groups), cholesterol, and cholesterol esters. Aside from their involvement in functions such as the maintenance of cell membranes and the manufacture of prostaglandins, lipids—primarily in the form of triglycerides—provide a stored source of energy. They are calorically dense molecules, providing more than twice the amount of energy (9 kcal) per gram as protein and carbohydrates.

Most dietary lipids—consisting primarily of triglycerides—are too large to be absorbed intact and are partially broken down (hydrolyzed) in the intestine to form monoglycerides and diglycerides, which contain one or two fatty acids, respectively, bound to glycerol.

Bile salts produced in the liver are detergents, and they promote the formation of micelles, which are emulsions of fatty acids, monoglycerides, and bile salts. Long-chain fatty acids, which contain more than 12 carbon atoms, are very insoluble in water; they are found mainly in the interior of the micelle. The external portion of the micelle, which includes the glycerol part of the triglycerides, is more water soluble than the interior portion. This allows the micelle to cross the unstirred water layer that coats the intestinal absorptive surface.

Inside the intestinal cells, monoglycerides and long-chain fatty acids rejoin to form triglycerides, and they are surrounded by phospholipids and specific proteins to form chylomicrons. These chylomicrons are transported out of the intestine through the lymphatic system, finally entering the blood circulation through the thoracic duct. Some of the chylomicrons are taken up by the liver, but most are directly transported to other tissues. Short-chain fatty acids (less than 8 carbon atoms long) and medium-chain fatty acids (8 to 12 carbon atoms long) are more water soluble than longer fatty acids; triglycerides containing these fatty acids can be absorbed without hydrolysis and are soluble enough to be transported to the liver through the portal vein, without chylomicron formation. Short- and medium-chain fatty acids have advantages in nutritional care of patients who have insufficient bile salt formation or inadequate intestinal surface area for absorption of long-chain fatty acids.

With the aid of the enzyme lipoprotein lipase, triglyceride-containing chylomicrons are broken down outside the cell and enter the cell as fatty acids and glycerol. Heparin stimulates lipoprotein lipase, and low doses of heparin are sometimes given to patients receiving intravenous lipid emulsions to improve lipid use. Insulin also stimulates the cellular uptake of triglycerides. Inside the cell, the fatty acids are oxidized (metabolized for energy) or reformed into triglycerides for storage. During an overnight fast, prolonged starvation, or metabolic stress when the carbohydrate supply is limited, the blood glucose level declines, and consequently, insulin levels decrease. In response, a process called lipolysis causes the breakdown of intracellular triglycerides, which provides fatty acids for energy production and glycerol for gluconeogenesis.

The fatty acids released from adipose tissue can be used by the liver, heart, or other tissues. In the liver, fatty acids are broken down to ketones (beta-hydroxybutyrate, acetoacetate, and acetone). In the absence of glucose, fatty acid breakdown and ketone production are increased. Ketones can be directly oxidized by skeletal muscle and used for energy. During prolonged starvation, the brain—which normally uses glucose—converts to using ketones as its primary energy source. This is a body defense mechanism to ensure a supply of energy when carbohydrate intake is low.

Assessing Nutritional Status

In the United States, The Joint Commission mandates nutrition screening be conducted on every patient within 24 hours of admission to an acute care center.1 A brief questionnaire to be completed by the patient or significant other, the nursing admission form, or the physician’s admission note usually provides enough information to determine whether the patient is at nutritional risk (Box 8-1). Any patient judged to be nutritionally at risk needs a more thorough nutrition assessment. The nutrition assessment process is continuous, with reassessments as a part of the overall nutrition care plan, as shown in Figure 8-1.2

Box 8-1   Patients Who are at Risk for Malnutrition

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FIGURE 8-1 Nutrition Care Process. (Redrawn from Mueller C, et al. A.S.P.E.N. Clinical guidelines, nutrition screening, assessment, and intervention in adults. JPEN J Parenter Enteral Nutr. 2009;33[1]:16.)

Nutrition assessment involves collection of four types of information: 1) anthropometric measurements; 2) biochemical (laboratory) data; 3) clinical signs (physical examination); and 4) diet and pertinent health history. This information provides a basis for 1) identifying patients who are malnourished or at risk of malnutrition; 2) determining the nutritional needs of individual patients; and 3) selecting the most appropriate methods of nutrition support for patients with or at risk of developing nutritional deficits. Nutrition support is the provision of specially formulated or delivered oral, enteral, or parenteral nutrients to maintain or restore optimal nutrition status.3 The nutrition assessment can be performed by or under the supervision of a registered dietitian or by a nutrition care specialist (e.g., nurse with specialized expertise in nutrition). Figure 8-2 shows the route of administration of specialized nutrition support.

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FIGURE 8-2 Route of Administration of Specialized Nutrition Support. (Redrawn from Ukleja A, et al. Standards for nutrition support. Nutrition in Clinical Practice. 2010;25[4]:403.)

Anthropometric Measurements

Height and current weight are essential anthropometric measurements, and they should be measured rather than obtained through a patient or family report. The most important reason for obtaining anthropometric measurements is to be able to detect changes in the measurements over time (e.g., track response to nutritional therapy). The patient’s measurements may be compared with standard tables of weight-for-height or standard growth charts for infants and children. Another simple and reliable tool for interpreting appropriateness of weight for height for adults and older adolescents is the body mass index (BMI).

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Weight is measured in kilograms and height in meters. BMI values are independent of age and gender and are used for assessing health risk. BMI can be classified as shown in Table 8-1.4,5 Evidence that the associations between BMI, percent of body fat, and body fat distribution differ across populations suggests the possible need for developing different BMI cut-off values for different ethnic groups.6 For example, alternate BMI classification cut-off values exist for Asians, who are at risk for obesity-related co-morbidities at lower BMI.6

TABLE 8-1

ADULT BMI CLASSIFICATIONS

CLASSIFICATION BMI (kg/m2)
Underweight <18.5
Normal 18.5-24.99
Overweight: ≥25
 Pre-obese 25-29.99
 Obese class I 30-34.99
 Obese class II 35-39.99
 Obese class III ≥40

From World Health Organization. Obesity: preventing and managing the global epidemic. Report of a WHO Consultation. WHO Technical Report Series 894. Geneva: World Health Organization; 2000.

It may be impossible to measure the height of some patients accurately. Total height can be estimated from arm span length or knee height.7,8 To measure knee height, bend the knee 90 degrees, and measure from the base of the heel to the anterior surface of the thigh.

For men:

height (cm)=64.19−(0.04×age in years)+(2.02×knee height [cm])

image

For women:

height (cm)=84.8−(0.24×age in years)+(1.83×knee height [cm])

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During critical illness, changes in anthropometric measures such as weight are more likely to reflect changes in body water and its distribution. Good judgment must be used in interpreting anthropometric data. For example, edema may mask significant weight loss or underweight. Despite these limitations, weight remains an important measure of nutritional status, and any recent weight change must be evaluated. A woman who was obese 4 months earlier and has lost 15 kg (33 lb) since then may be at nutritional risk even if her current weight is appropriate for her height.

In addition to height and weight data, other measurements such as arm muscle circumference, skin fold thickness, and body composition (proportion of fat and lean tissue, determined by bioelectric impedance or other methods) are sometimes performed, but these measurements are of limited use in assessing critically ill patients.9

Biochemical Data

A wide range of laboratory tests can provide information about nutritional status. Those most often used in the clinical setting are described in Table 8-2. No diagnostic tests for evaluation of nutrition are perfect, and care must be taken in interpreting the results of the tests.10

TABLE 8-2

COMMON BLOOD AND URINE TESTS USED IN NUTRITION ASSESSMENT

TEST COMMENTS AND LIMITATIONS
Serum Proteins  
Albumin or prealbumin Levels decrease with protein deficiency and in liver failure. Albumin levels are slow to change in response to malnutrition and repletion. Prealbumin levels fall in response to trauma and infection.
Hematologic Values  
Anemia  
Normocytic (normal MCV, MCHC) Common with protein deficiency
Microcytic (decreased MCV, MCH, MCHC) Indicative of iron deficiency (can be from blood loss)
Macrocytic (increased MCV) Common in folate and vitamin B12 deficiency
Lymphocytopenia Common in protein deficiency

MCH, Mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume.

Clinical or Physical Manifestations

A thorough physical examination is an essential part of nutrition assessment. Box 8-2 lists some of the more common findings that may indicate an altered nutritional state. It is especially important for the nurse to check for signs of muscle wasting, loss of subcutaneous fat, skin or hair changes, and impairment of wound healing.

Box 8-2   Clinical Manifestations of Nutritional Alterations

Diet and Health History

Information about dietary intake and significant variations in weight is a vital part of the history. Dietary intake can be evaluated in several ways, including a diet record, a 24-hour recall, and a diet history. The diet record, a listing of the type and amount of all foods and beverages consumed for some period (usually 3 days), is useful for evaluating the patient’s intake in the critical care setting if the adequacy of intake is questionable. However, such a record reveals little about the patient’s habitual intake before the illness or injury. The 24-hour recall of all food and beverage intake is easily and quickly performed, but it also may not reflect the patient’s usual intake and has limited usefulness. The diet history consists of a detailed interview about the patient’s usual intake, along with social, familial, cultural, economic, educational, and health-related factors that may affect intake. Although the diet history is time consuming to perform and may be too stressful for the acutely ill patient, it does provide a wealth of information about food habits over a prolonged period and a basis for planning individualized nutrition education if changes in eating habits are desirable. Other information to include in a nutrition history is listed in Box 8-3.

Box 8-3   Nutrition History Information

Determining Nutritional Needs

A variety of methods can be used in clinical practice to estimate caloric requirements. Indirect calorimetry, a method by which energy expenditure is calculated from oxygen consumption (Vo2) and carbon dioxide production (Vco2), is the most accurate method for determining caloric needs.11,12 Indirect calorimetry is useful in those patients suspected to have a high metabolic rate. This test can also analyze substrate use, which can be extrapolated from VO2 and VCO2 during a steady state of respiration. The respiratory quotient (RQ) is equal to the VCO2 divided by the Vo2. Fat, protein, and carbohydrates each have a unique RQ, thus RQ identifies which substrate is being preferentially metabolized and may provide target goals for calorie replacement.12 For example, the RQ for the metabolism of fats is about 0.7 while the RQ for the metabolism of carbohydrates is 1.0. A mixed fuel diet results in an RQ of approximately 0.8.12 The test can be performed on spontaneously breathing patients and on those who require mechanical ventilation. Some ventilators are constructed so that they can perform indirect calorimetry. However, for most patients, indirect calorimetry requires the use of a metabolic cart, which is not available in all institutions. To maintain accuracy and reliability of measurement, several testing criteria must be met.12 Information received from the metabolic cart is limited; measurements are conducted over a relatively brief period (often 20 to 30 minutes) and may not be representative of energy expenditure over the whole day.

Calorie and protein needs of patients are often estimated using formulas that provide allowances for increased nutrient use associated with injury and healing. Although indirect calorimetry is considered the most accurate method to determine energy expenditure, estimates using formulas have demonstrated reasonable accuracy.13–15 Commonly used formulas for critically ill patients can be found in Appendix B. Some rules of thumb are available to provide a rough estimate of caloric needs so that nurses and other caregivers can quickly determine if patients are being seriously overfed or underfed (Table 8-3).

TABLE 8-3

ESTIMATING ENERGY NEEDS

CATEGORY DESCRIPTION CALORIES/kg CALORIES/lb
Obese More than 40% over ideal body weight or BMI >30 21 9.5
Sedentary Relatively inactive individual without regular aerobic exercise; hospitalized patient without severe injury or sepsis 25-30 11-13.5
Moderate activity or injury Individual obtaining regular aerobic exercise plus routine activities; patient with trauma or sepsis 30-35 13.5-16
Very active or severe injury Manual laborer or athlete in very active training; patient with major burns or trauma 40 18

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The goal of nutrition assessment is to obtain the most accurate estimate of nutritional requirements. Underfeeding and overfeeding must be avoided during critical illness. Overfeeding results in excessive production of carbon dioxide, which can be a burden in the person with pulmonary compromise. Overfeeding increases fat stores, which can contribute to insulin resistance and hyperglycemia. Hyperglycemia increases the risk of postoperative infections in diabetic and nondiabetic individuals.16

Implications of Undernutrition for the Sick or Stressed Patient

As many as 40% of hospitalized patients are at risk for malnutrition.17–20 Although illness or injury is the major factor contributing to development of malnutrition, other possible contributing factors are lack of communication among the nurses, physicians, and dietitians responsible for the care of these patients; frequent diagnostic testing and procedures, which lead to interruption in feeding; medications and other therapies that cause anorexia, nausea, or vomiting and thereby interfere with food intake; insufficient monitoring of nutrient intake; and inadequate use of supplements, tube feedings, or parenteral nutrition to maintain the nutritional status of these patients.

Nutritional status tends to deteriorate during hospitalization unless appropriate nutrition support is started early and continually reassessed. Malnutrition in hospitalized patients is associated with a wide variety of adverse outcomes. Wound dehiscence, pressure ulcers, sepsis, infections, respiratory failure requiring ventilation, longer hospital stays, and death are more common among malnourished patients.21–23 Decline in nutritional status during hospitalization is associated with higher incidences of complications, increased mortality rates, increased length of stay, and higher hospital costs.

It is rare for a patient to exhibit a lack of only one nutrient. Nutritional deficiencies usually are combined, with the patient lacking adequate amounts of protein, calories, and possibly vitamins and minerals.

Energy Deficiency

Protein-Calorie Malnutrition

Malnutrition results from the lack of intake of necessary nutrients or improper absorption and distribution of them, as well as from excessive intake of some nutrients. Malnutrition can be related to any essential nutrient or nutrients, but a serious type of malnutrition found frequently among hospitalized patients is protein-calorie malnutrition (PCM). Poor intake or impaired absorption of protein and energy from carbohydrate and fat worsens the debilitation that may occur in response to critical illness. In PCM, the body proteins are broken down for gluconeogenesis, reducing the supply of amino acids needed for maintenance of body proteins and healing. Malnutrition can be caused by simple starvation—the inadequate intake of nutrients (e.g., in the patient with anorexia related to cancer). It also can result from an injury that increases the metabolic rate beyond the supply of nutrients (hypermetabolism). In the seriously ill patient, if malnutrition occurs, usually it is the result of the combined effects of starvation and hypermetabolism. Two types of PCM are kwashiorkor and marasmus.

Kwashiorkor results in low levels of the serum proteins albumin, transferrin, and prealbumin; low total lymphocyte count; impaired immunity; loss of hair or hair pigment; edema resulting from low plasma oncotic pressure caused by a loss of plasma proteins; and an enlarged, fatty liver. Marasmus is recognizable by weight loss, loss of subcutaneous fat, and muscle wasting. In the marasmic person, creatinine excretion in the urine is low, an indication of reduced muscle mass. Because PCM weakens muscles, increases vulnerability to infection, and can prolong hospital stays, the health care team should diagnose this serious disorder as quickly as possible so that an appropriate nutrition intervention can be implemented.

Metabolic Response to Starvation and Stress

To understand the development of malnutrition in the hospitalized patient, the nurse must understand the metabolic response to starvation and physiologic stress. Changes in endocrine status and metabolism together determine the onset and extent of malnutrition. Nutritional imbalance occurs when the demand for nutrients is greater than the exogenous nutrient supply. The major difference between a person who is starved and one who is starved and injured is that the latter has an increased reliance on tissue protein breakdown to provide precursors for glucose production to meet increased energy demands. Although carbohydrate and fat metabolism are also affected, the main concern is about protein metabolism and homeostasis.

During an acute, nonstressed fast, blood levels of glucose and insulin fall, and glucagon levels rise. Glucagon stimulates the liver to release glucose from its glycogen reserves, which become exhausted within a few hours. Glucagon also stimulates gluconeogenesis, and skeletal muscle provides a large amount of the substrates required for gluconeogenesis. As fasting progresses, fat becomes the primary source of fuel, and the blood ketone levels begin to increase. After the circulating ketone level rises, the brain is able to use ketones for 70% of its energy, thereby decreasing the total body’s reliance on glucose as an energy source. As gluconeogenesis from protein precursors decreases, protein breakdown and nitrogen excretion also slow. Some tissues, such as red blood cells, the renal medulla, and 30% of brain cells, are obligatory glucose users, and they continue to require a small amount of amino acids for gluconeogenesis. However, endogenous protein stores are spared from use for gluconeogenesis to a major extent, and protein homeostasis is partially restored.

Critically ill patients are at risk for a combination of starvation and the physiologic stress resulting from injury, trauma, major surgery, or sepsis. Starvation occurs because the person must have nothing by mouth (NPO) for surgical procedures, is unable to eat because of disease-related factors, or is hemodynamically too unstable to be fed. The physiologic stress causes an increased metabolic rate (hypermetabolism) that results in increased oxygen consumption and energy expenditure.

The hypermetabolic process results from increased catabolic hormone changes caused by the stressful event. The sympathetic nervous system is stimulated, causing the adrenal medulla to release catecholamines (epinephrine and norepinephrine). Other hormones released in response to stress include glucagon, adrenocorticotropic hormone (ACTH), antidiuretic hormone (ADH), and glucocorticoids and mineralocorticoids (e.g., cortisol, aldosterone). Cytokines are peptide messengers secreted by macrophages as part of the inflammatory response, and they serve as hormonal regulators of the immune system. Cytokine levels increase in response to sepsis and trauma. Important cytokines include tumor necrosis factor (TNF), cachectin, interleukin 1 (IL-1), and interleukin 6 (IL-6). All of these hormonal changes cause nutrient substrates, primarily amino acids, to move from peripheral tissues (e.g., skeletal muscle) to the liver for gluconeogenesis.

Unfortunately, this mobilization of substrates occurs at the expense of body tissue and function at a time when the needs for protein synthesis (e.g., wound healing, acute-phase proteins) also are high. Hyperglycemia results from the effects of increased catecholamines, glucocorticoids, and glucagon. The body relies on its protein stores to provide substrates for gluconeogenesis, because glucose becomes the major fuel source. Loss of protein results in a negative nitrogen balance and weight loss. Catabolism may be unresponsive to nutrient intake.

Nutrition Support

Nursing Management of Nutrition Support

Nutrition support is an important aspect of the care of critically ill patients. Maintenance of optimal nutritional status may prevent or reduce the complications associated with critical illness and promote positive clinical outcomes.3 Critical care nurses play a key role in the delivery of nutrition support and must work closely with dietitians and physicians in promoting the best possible outcomes for their patients.

Nutrition support is the provision of oral, enteral, or parenteral nutrients. It is an essential adjunct in the prevention and management of malnutrition in critically ill patients.3 The goal of nutrition support therapy is to provide enough support for body requirements, to minimize complications, and to promote rapid recovery. Critical care nurses must have a broad understanding of nutrition support, including the indications, prevention, and management of associated complications.

Oral Supplementation

Oral supplementation may be necessary for patients who can eat and have normal digestion and absorption but cannot consume enough regular foods to meet caloric and protein needs. Patients with mild to moderate anorexia, burns, or trauma sometimes fall into this category. To improve intake and tolerance of supplements, there are several steps for the critical care nurse to take:

1. Collaborate with the dietitian to choose appropriate products and allow the patient to participate in the selection process, if possible. Milk shakes and instant breakfast preparations are often more palatable and economical than commercial supplements. However, lactose intolerance is common among adults. Many disease processes (e.g., Crohn’s disease, radiation enteritis, human immunodeficiency virus [HIV] infection, severe gastroenteritis) can cause lactose intolerance. Individuals with this problem require commercial lactose-free supplements or milk treated with lactase enzyme.

2. Offer to serve commercial supplements well chilled or on ice, because this improves flavor.

3. Advise patients to sip formulas slowly, consuming no more than 240 mL over 30 to 45 minutes. These products contain easily digestible carbohydrates. If formulas are consumed too quickly, rapid hydrolysis of the carbohydrate in the duodenum can contribute to dumping syndrome, characterized by abdominal cramping, weakness, tachycardia, and diarrhea.

4. Record all supplement intake separately on the intake-and-output sheet so that it can be differentiated from intake of water and other liquids.

Enteral Nutrition

Enteral nutrition or tube feedings are used for patients who have at least some digestive and absorptive capability but are unable or unwilling to consume enough by mouth. When possible, the enteral route is the preferred method of feeding over total parenteral nutrition (TPN). The proposed advantages of enteral nutrition over TPN include lower cost, better maintenance of gut integrity, and decreased infection and hospital length of stay.3 A review of the literature comparing enteral nutrition and TPN indicates that enteral nutrition is less expensive than TPN and is associated with a lower risk of infection.3,24

The gastrointestinal (GI) tract plays an important role in maintaining immunologic defenses, which is why nutrition by the enteral route is thought to be more physiologically beneficial than TPN. Some of the barriers to infection in the GI tract include neutrophils; the normal acidic gastric pH; motility, which limits GI tract colonization by pathogenic bacteria; the normal gut microflora, which inhibit growth of or destroy some pathogenic organisms; rapid desquamation and regeneration of intestinal epithelial cells; the layer of mucus secreted by GI tract cells; and bile, which detoxifies endotoxin in the intestine and delivers immunoglobulin A (IgA) to the intestine. A second line of defense against invasion of intestinal bacteria is the gut-associated lymphoid tissue (GALT).25 The systemic immune defenses in the GI tract are stimulated by the presence of food within it. In animal models, resting the GI tract by providing TPN contributes to bacterial translocation, whereby bacteria normally found in the GI tract cross the intestinal barrier, are found in the regional mesenteric lymph nodes, and give rise to generalized sepsis. However, there is insufficient evidence in humans that TPN causes atrophy of the intestinal mucosa or that enteral nutrition prevents bacterial translocation.26,27

Patients who are experiencing severe stress that greatly increases their nutritional needs (caused by major surgery, burns, or trauma) often benefit from tube feedings. Table 8-4 lists different enteral formula types and the nutritional indications for using each one. Individuals who require elemental formulas because of impaired digestion or absorption or the specialized formulas for altered metabolic conditions usually require tube feeding because the unpleasant flavors of the free amino acids, peptides, or protein hydrolysates used in these formulas are very difficult to mask if taken in orally.

TABLE 8-4

ENTERAL FORMULAS

FORMULA TYPE NUTRITIONAL USES CLINICAL EXAMPLES EXAMPLES OF COMMERCIAL PRODUCTS (MANUFACTURER)
Formulas Used When GI Tract Is Fully Functional
Polymeric (standard): Contains whole proteins (10%-15% of calories), long-chain triglycerides (25%-40% of calories), and glucose polymers or oligosaccharides (50%-60% of calories); most provide 1 calorie/mL Inability to ingest food
Inability to consume enough to meet needs		 Oral or esophageal cancer
Coma, stroke
Anorexia resulting from chronic illness
Burns or trauma

High-nitrogen: Same as polymeric except protein provides >15% of calories Same as polymeric plus mild catabolism and protein deficits Trauma or burns
Sepsis Concentrated: Same as polymeric except concentrated to 2 calorie/mL Same as polymeric but fluid restriction needed Heart failure
Neurosurgery
COPD
Liver disease Formulas Used When GI Function Is Impaired Elemental or predigested: Contains hydrolyzed (partially digested) protein, peptides (short chains of amino acids), and/or amino acids, little fat (<10% of calories) or high MCT, and glucose polymers or oligosaccharides; most provide 1 calorie/mL Impaired digestion and/or absorption Short bowel syndrome
Radiation enteritis
Inflammatory bowel disease Diets for Specific Disease States* Renal failure: Concentrated in calories; low sodium, potassium, magnesium, phosphorus, and vitamins A and D; low protein for renal insufficiency; higher protein formulas for dialyzed patients Renal insufficiency
Dialysis Predialysis
Hemodialysis or peritoneal dialysis Hepatic failure: Enriched in BCAA; low sodium Protein intolerance Hepatic encephalopathy Pulmonary dysfunction: Low carbohydrate, high fat, concentrated in calories Respiratory insufficiency Ventilator dependence Glucose intolerance: High fat, low carbohydrate (most contain fiber and fructose) Glucose intolerance Individuals with diabetes mellitus whose blood sugar is poorly controlled with standard formulas Critical care, wound healing: High protein; most contain MCT to improve fat absorption; some have increased zinc and vitamin C for wound healing; some are high in antioxidants (vitamin E, beta-carotene); some are enriched with arginine, glutamine, and/or omega-3 fatty acids Critical illness Severe trauma or burns
Sepsis

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BCAA, Branched chain–enriched amino acid; COPD, chronic obstructive pulmonary disease; GI, gastrointestinal; MCT, medium-chain triglyceride.

*These diets may be beneficial for selected patients; costs and benefits must be considered.

Immune-enhancing formulas (IEFs) have emerged as a means to protect and stimulate the immune system. Some of the enterally delivered nutrients that may benefit critically ill patients include fiber, the amino acids glutamine and arginine, the omega-3 (n-3) fatty acids, and the nucleotide ribonucleic acid (RNA).28 Fiber is not digested by humans but can be metabolized by gut bacteria to yield short-chain fatty acids, the primary fuel of the colon cells. Glutamine is the major fuel of the small intestinal cells. It is considered a nonessential amino acid, but it becomes conditionally essential in illness. It has been shown to improve mortality and infectious morbidity in critically ill patients.29–31 Arginine is involved in protein synthesis and is a precursor of nitric oxide, a molecule that stimulates vasodilation in the GI tract and heart and mediates hepatic protein synthesis during sepsis.28 The omega-3 fatty acids, derived primarily from fish oils, are involved in synthesis of eicosanoids (molecules with hormone-like activity)—prostaglandins, prostacyclin, and leukotrienes—and may modulate the inflammatory response.

There are a variety of commercial enteral feeding products, some of which are designed to meet the specialized needs of the critically ill. Products designed for the stressed patient with trauma or sepsis are usually rich in glutamine, arginine, branched amino acids (a major fuel source, especially for muscle), and antioxidant nutrients, such as selenium and vitamins C, E, and A.32 The antioxidants help to reduce oxidative injury to the tissues (e.g., from reperfusion injury). Despite the fact that IEFs may reduce the incidence of infectious complications, the efficacy and safety of these formulas in critically ill patients have not been clearly demonstrated.33–36

Early enteral nutrition, administered with the first 24 to 48 hours of critical illness, has been advocated as a way to reduce septic complications and improve feeding tolerance in critically ill patients. Although studies37 have shown a lower risk of infection and decreased length of stay with early enteral nutrition, the benefit of early enteral nutrition compared with enteral nutrition delayed a few days remains controversial.3,38 Current guidelines support the initiation of nutrition support in critically ill patients who will be unable to meet their nutrient needs orally for a period of 5 to 10 days.3 To avoid complications associated with intestinal ischemia and infarction, enteral nutrition must be initiated only after fluid resuscitation and adequate perfusion have been achieved.39,40

Critically ill patients may not tolerate early enteral feeding because of impaired gastric motility, ileus, or medications administered in the early phase of illness. This is particularly true for patients receiving gastric enteral feeding.41 The assessment of enteral feeding tolerance is an important aspect of nursing care. Monitoring of gastric residual volume is a method used to assess enteral feeding tolerance. However, evidence suggests that gastric residuals are insensitive and unreliable markers of tolerance to tube feeding.42 There is little evidence to support a correlation between gastric residual volumes and tolerance to feedings, gastric emptying, and potential aspiration. Except in selected high-risk patients, there is little evidence to support holding tube feedings in patients with gastric residual volumes less than 400 mL.42 The gastric residual volume should be evaluated within the context of other gastrointestinal symptoms. Prokinetic agents, including metoclopramide and erythromycin, have been used to improve gastric motility and promote early enteral nutrition in critically ill patients.43–45

Enteral Feeding Access. 

Achievement of enteral access is the cornerstone of enteral nutrition therapy. Several techniques can be used to facilitate enteral access. These include surgical methods, bedside methods, fluoroscopy, endoscopy, air insufflation, and prokinetic agents.9 Placement of feeding tubes beyond the stomach (postpyloric) eliminates some of the problems associated with gastric feeding intolerance. However, placement of postpyloric feeding tubes is time-consuming and may be costly. Tubes with weights on the proximal end are available; they were originally designed for postpyloric feeding in the belief that that they would be more likely than unweighted tubes to pass spontaneously through the pyloric sphincter. However, randomized trials with the two types of tubes have shown that unweighted tubes are more likely to migrate through the pylorus than weighted tubes.46 The weights sometimes cause discomfort while being inserted through the nares. Unweighted tubes therefore may be preferable.

After the tube is placed, correct location must be confirmed before feedings are started and regularly throughout the course of enteral feedings. Radiographs are the most accurate way of assessing tube placement, but repeated radiographs are costly and can expose the patient to excessive radiation. After correct placement has been confirmed, marking the exit site of the tube to check for movement is helpful. Alternative methods for confirming tube placement have been researched that attempt to verify placement in the stomach or small intestine. An inexpensive and relatively accurate alternative method involves assessing the pH of fluid removed from the feeding tube; some tubes are equipped with pH monitoring systems. Assessing the pH and the bilirubin concentration in fluid aspirated from the feeding tube is a newer method for confirming tube placement.47

Location and Type of Feeding Tube. 

Decisions regarding enteral access should be determined based on gastrointestinal anatomy, gastric emptying, and aspiration risk.3 Nasal intubation is the simplest and most commonly used route for enteral access. This method allows access to the stomach, duodenum, or jejunum. Tube enterostomy—a gastrostomy or jejunostomy—is used primarily for long-term feedings (6 to 12 weeks or more) and when obstruction makes the nasoenteral route inaccessible. Tube enterostomies may also be used for the patient who is at risk for tube dislodgment because of severe agitation or confusion. A conventional gastrostomy or jejunostomy is often performed at the time of other abdominal surgery. The percutaneous endoscopic gastrostomy (PEG) tube has become extremely popular because it can be inserted at the bedside without the use of general anesthetics. Percutaneous endoscopic jejunostomy (PEJ) tubes are also used.

Postpyloric feedings through nasoduodenal, nasojejunal, or jejunostomy tubes are commonly used when there is a high risk of pulmonary aspiration, because the pyloric sphincter theoretically provides a barrier that lessens the risk of regurgitation and aspiration.48 However, some studies have demonstrated that gastric feeding is safe and not associated with an increased risk of aspiration.49–51 Postpyloric feedings have an advantage over intragastric feedings for patients with delayed gastric emptying, such as those with head injury, gastroparesis associated with uremia or diabetes, or postoperative ileus. Delivery of enteral nutrition into the small bowel is associated with improved tolerance,52 higher calorie and protein intake,53 and fewer gastrointestinal complications.41 Small bowel motility returns more quickly than gastric motility after surgery, and it is often possible to deliver transpyloric feedings within a few hours of injury or surgery.48 Figure 8-3 shows the locations of tube feeding sites.

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