Nutrition Support For Malnourished, Acutely Ill Adults

Nutrition Support For Malnourished, Acutely Ill Adults

Sybil Bowers


This independent study offering is designed for nurses and other health care professionals who care for and educate malnourished, acutely ill adult patients. The multiple choice examination that follows is designed to test your achievement of the following educational objectives. After studying this offering, you will be able to:

1. Identify the effects of malnutrition on the acutely ill adult.

2. Discuss the components of a nutritional assessment.

3. Define the fundamental principles of nutritional support.

4. Describe the nurse’s role in providing enteral and parenteral nutrition to the acutely ill adult.

5. Identify potential complications associated with enteral and parenteral nutrition therapies.

Why is nutrition support important for the acutely ill adult? Because malnutrition is never in the patient’s best interest. Unfortunately, malnutrition is not a new or rare problem. More than 15 million people are treated annually in American hospitals for illnesses, injuries, and socioeconomic problems which place them at high risk for malnutrition. In studies involving 1,327 hospitalized adults, 40% to 55% were malnourished or at risk for malnutrition (Gallagher-Allred, Voss, Finn, & McCamish, 1996). Up to 12% of these patients were severely malnourished. It has been clearly demonstrated that malnourished patients have increased morbidity and mortality rates. Malnourished surgical patients are two to three times more likely to have minor and major complications, increased mortality rates, and increased length of stay (LOS) (up to 90% longer than well-nourished patients). When compared to well-nourished patients, malnourished patients of all ages have higher costs associated with hospitalization. Hospital charges may be 35% to 75% higher due to increased morbidity, negative outcomes, increased LOS and increased use of resources for treating complications associated with malnutrition (Gallagher-Allred et al., 1996).

There are many reasons for the high prevalence of malnutrition in hospitalized adults. Some are unavoidable and are the consequence of catabolic diseases such as cancer or AIDS (see Table 1). Malnutrition occurs in all diagnosis groups and often worsens after prolonged hospitalization. However, it should not occur from lack of early recognition or from the absence of access to appropriate medical nutrition therapies (Gallagher-Allred et al., 1996).

Table 1.

Catabolic Disease States

* Trauma

* Burns


* Diabetes

* Renal failure

* Cancer


Malnutrition results from a variety of abnormal clinical conditions related to nutrient intake, digestion, absorption, metabolism, and excretion. If total energy and protein requirements are not met with the minimal daily intake of essential protein, carbohydrates, fats, minerals, trace elements, and vitamins, nutritional deficiencies will develop. Malnutrition develops rapidly in the presence of acute illness, stress, and injury. Malnourished patients are at greater risk for infection, organ failure, decreased wound healing, and suboptimal response to medical treatment (American Society of Parenteral and Enteral Nutrition [ASPEN], 1993).

As the acuity of hospitalized patients increases, so does the need for nurses to become more knowledgeable about nutritional support for the acutely ill. To provide safe and comprehensive care, nurses must recognize malnutrition and intervene in a timely manner to avoid adverse consequences. Nurses are responsible for assessing the patient’s risk factors, performing a physical assessment, observing for signs and symptoms of malnutrition, administering nutrition support therapies, assessing for possible complications, and monitoring the effectiveness of nutritional interventions (Shuster, 1994). Early nutritional assessment and appropriate nutrition support by an intradisciplinary health care team or nutrition support team is essential for delivering quality health care. Appropriate and timely nutrition support can address the problem of malnutrition, improve clinical outcomes, and reduce the costs of health care (Gallagher-Allred et al., 1996).

Types of Malnutrition

Several types of malnutrition are seen in American hospitals today. Amazingly, kwashiorkor, marasmus, and mixed-types of malnutrition are not uncommon. Kwashiorkor occurs when the diet contains various amounts of nonprotein calories (inadequate, adequate, or excessive) from carbohydrates and fats, but is deficient in total protein and essential amino acids. The patient’s weight is less than 90% of the ideal body weight. Laboratory tests show transferrin [is less than] 200 mg/dl or albumin [is less than] 3.5 g/dl. The patient may verbalize a history of decreased oral intake, anorexia, nausea, and/or vomiting greater than 2 weeks. Skeletal muscle mass and body fat are usually normal, but may be slightly depleted. The patient may not appear unusually thin, but is malnourished due to protein depletion. Kwashiorkor is commonly seen in patients with a history of alcohol abuse or intravenous drug abuse. The patient experiences generalized or dependent edema from hypoalbunemia, sodium retention, and decreased serum osmolality. There is a poor insulin response to glucose load, possibly due to chromium deficiency. The patient may have a “flaky paint” dermatosis, apathetic affect, thin and discolored hair, and an enlarged, fatty liver (Berkow & Fletcher, 1992; Ziegler & Filer, 1996).

Marasmus is the most common nutritional deficiency observed in American hospitalized patients. This protein-calorie malnutrition (PCM) is characterized by depletion of muscle, visceral protein stores, and body fat. The patient’s oral diet may include an acceptable protein:calorie ratio but is inadequate in quantity and calories. Energy intake is insufficient to meet the nutritional requirements and the body draws on its own stores. During physical assessment, the nurse observes dependent edema, marked wasting of body adipose and skeletal muscle tissue, and dramatic weight loss. Weight will be less than 90% of ideal or usual body weight. The patient complains of a history of unplanned weight loss in the last 6 months, decreased oral intake, anorexia, nausea, vomiting, and/or diarrhea for more than 2 weeks. Transferrin level is [is less than] 200 mg/dl and serum albumin is [is less than] 3.5 g/dl. Clinical manifestations include increased morbidity and mortality, impaired wound healing, and compromised immune response (Berkow & Fletcher, 1992; Grant, 1992; Mears, 1996; Ziegler & Filer, 1996.)

Marasmic-kwashiorkor is a mixed form of any PCM symptoms. It frequently occurs when the marasmic patient experiences the catabolic stress of illness or trauma. The patient may be admitted to the hospital with a pre-existing marasmus related to a disease process, then develops an iatrogenic kwashiorkor due to lack of oral intake and/or nutritional support. For example, administering a clear liquid diet or intravenous hydration without additional necessary nutrients for 5 to 7 days predisposes the patient to developing PCM. The average clear liquid hospital diet contains less than 1,000 kcal/day and the protein content meets only 3.7% of the recommended daily requirement (Jastram, 1998). Symptoms of marasmic-kwashiorkor may include electrolyte depletion (especially potassium and magnesium), iron deficiency anemia, dehydration, and diarrhea in combination with any other clinical manifestations of PCM.

Prolonged starvation causes numerous problems (see Figure 1). During periods of prolonged starvation there is a gradual decrease in total body energy expenditure, including a decreased metabolic rate, diminished muscle activity, increased sleep, and decreased core temperature. The need for gluconeogenesis diminishes, mainly as a result of the central nervous system’s conversion to utilization of ketone bodies for energy rather than glucose. Protein catabolism drops from 75 g/day to 20 g/day, which is associated with a marked decrease in excretion of urea nitrogen. In a fully adapted state of starvation, protein catabolism provides as little as 5% of the total daily calories. When gluconeogenesis decreases, adipose tissue becomes a more important energy substrate, as follows: 60% of total caloric expenditure is derived from metabolism of fat to carbon dioxide; 10% from conversion of free fatty acids to ketone bodies; and 25% from metabolism of ketone bodies by peripheral tissues. Increased fat metabolism causes increased serum ketone body concentrations which eventually exceed the renal threshold.


The appearance of ketones in the urine is the hallmark physiologic response to prolonged starvation. Metabolic acidosis is not present. Humans may be able to tolerate prolonged fasting (up to 60 to 70 days) in this fully adapted state. Death will occur after about 60 days of simple starvation; the process is accelerated in hypermetabolic hospitalized patients with increased caloric requirements (see Figure 2). During recovery from starvation, essential amino acid, total protein, and caloric requirements are all greater than normal. After nitrogen losses are restored, fat is gained for several weeks or months until the normal body fat stores are regained. In this phase nitrogen balance is zero. It is possible to calculate the approximate time required for metabolic recovery by dividing the estimated total protein deficit by the average daily gain. However, the actual time required to replace all protein losses is somewhat longer than calculated because maximum anabolism is not immediately or consistently obtained (Grant, 1992).


Fundamental Principles of Nutrition Support

There are five general principles concerning malnutrition that guide clinical care known as Grant’s Principles of Malnutrition (Grant, 1992). Although based on common sense, they provide direction for providing nutritional support for acutely ill patients.

Principle I. No disease benefits from starvation or from infusion of only 5% dextrose solutions. If the diet is significantly inadequate for more than a few days, catabolism of body protein mass begins to cause harm by inducing organ dysfunction with increased morbidity and mortality. The standard intravenous solution of 100 to 150 grams glucose in an electrolyte solution does not meet minimal requirements for a 24-hour period, much less for days or weeks.

Principle II. Progressive malnutrition leads to vital organ wasting with impairment of function.

Principle III. Increasing malnutrition is associated with increased morbidity and mortality. Death is inevitable if starvation lasts sufficiently long. Classic studies demonstrated that patients undergoing elective procedures for peptic ulcer disease had a mortality rate of 3.5% if they had less than a 20% loss of body weight pre-operatively (Grant, 1992). However, when more than 20% of body weight was lost pre-operatively, there was a tenfold increase in mortality. As malnutrition progresses, the nurse will observe lethargy, followed by hypothermia, bradycardia, altered immune function, vital organ failure, and eventually death. Death from starvation occurs at approximately 30 days for patients under moderate stress and at approximately 15 days for patients suffering severe stress and is typically reported to have been caused by multiple system organ failure. When an acutely ill patient suffers from moderate to severe stress and survival days are limited, nutritional support should not be delayed. If a patient is well nourished but is scheduled to undergo a major operative procedure which will place him under severe stress and will require a prolonged period before an oral diet is resumed, nutrition support should be started early to prevent complications of malnutrition. The clinician’s goal is to optimize outcome, not to try to salvage the patient who has been allowed to become malnourished.

Principle IV. The primary goal of nutritional support is the maintenance and repletion of nutritional status. Secondary goals include improving the response to treatments, prolonging survival, decreasing complications, and allowing for earlier discharge from the intensive care unit or hospital. These secondary goals are meritorious but difficult to measure in direct relationship to nutrition support. If the value of nutritional support is measured by the primary goal, it is nearly always an effective therapy.

Principle V. Nutritional support should begin early before malnutrition develops, or as soon as possible thereafter. Clinicians spend much time identifying the presence and severity of malnutrition. However, once malnutrition is present, the patient is already subject to increased morbidity and mortality. If optimal care is to be given, nurses and other health care providers must make every effort to identify patients at risk of developing malnutrition before malnutrition is present and promptly institute nutritional support.

Obviously, morbidity and mortality are not solely dependent upon nutrition. There are some disease processes in which the patient does not benefit from nutritional support. Some patients may be too near death for nutritional intervention to be of any value. Other patients become “chronically critical,” dependent on the intensive care environment for survival, unable to be weaned from life support, yet unable to die as long as full support is continued. The intradisciplinary health care team must carefully evaluate patients in this unfortunate situation in an ethical and humane manner. In these end-of-life situations, it is sometimes the most compassionate and wise decision to recognize that nutrition support will not provide any benefit and will only extend suffering.

How to Feed Patients

An intradisciplinary team or nutrition support team (including a nurse, physician, dietician, and pharmacist) develops a comprehensive plan for nutrition support therapy to minimize possible complications and promote optimal patient outcome. The nurse is a key member of the team, acting as the patient’s advocate and using the nursing process to assess, plan, implement, and evaluate care. The following plan may be used to provide high-quality nutritional support to the acutely ill, malnourished adult (see Table 2).

Table 2. How to Feed Your Patients

* Assess patient for evidence of malnutrition.

* Calculate energy and protein needs.

* Establish method of feeding.

* Select access route for nutrition delivery.

* Select formula (enteral or parenteral).

* Establish method of delivery.

* Monitor for complications.

* Avoid refeeding syndrome.

Assess the Patient for Evidence of Malnutrition or Nutritional Risk

Components of a nutritional assessment. Nutritional assessment follows a standardized protocol. Clinicians identify malnourished patients by using nutritional assessment techniques which are readily available and relatively inexpensive. There is no universally accepted index of nutritional status, but the experienced clinician will use a variety of indicators to evaluate the presence or risk of malnutrition. The expertise of the health care team members, laboratory capability, cost, and patient population will determine the selection of initial screening and followup assessment tools. Generally, the evaluation will include a history, physical examination, laboratory data, overall nutritional assessment, calculation of nutrient needs, and followup evaluations. Patient data obtained during the assessment are predictive of morbidity, mortality, and response to medical therapies. For example, weight loss is highly predictive for hospital readmission and increased mortality rates for geriatric patients. Poor functional status, serum albumin levels below 3.5 g/dl, and the presence of renal or pulmonary disease are associated with increased morbidity among geriatric patients (Gallagher-Allred et al., 1996; Grant, 1992).

There is no single laboratory test which is a totally reliable indicator of PCM. A laboratory profile (total protein level, serum albumin, hematocrit, and lymphocyte count) provides cost-effective biochemical markers. Albumin is the traditional marker for PCM and is useful for identifying the chronic state of malnutrition. However, in the acutely ill adult, albumin is too insensitive to monitor nutritional therapies and assess current PCM status, due to the 20-day half-life and sensitivity to the patient’s hydration status. Transferrin is also a less accurate measurement during acute illness because it has an 8-day half-life and is sensitive to the patient’s iron status. Prealbumin, also known as transthyretin, is a more appropriate nutritional marker in the acutely ill adult because it has a 2-day half-life. It is a useful indicator of nutritional status and effectiveness of therapy because the concentration of transthyretin is greatly decreased in patients with PCM and tends to return to normal with nutritional repletion. Prealbumin is preferred over retinol-binding protein because it is easily quantified on existing laboratory instrumentation and is less affected by liver disease (see Table 3). Other nutritional assessment labwork may include a complete blood count, electrolytes, blood urea nitrogen, creatinine, glucose, calcium, phosphorus, magnesium, zinc lipid panel, and liver function tests (Gallagher-Allred et al., 1996; Grant, 1992; Mears, 1996).

Table 3. Laboratory Values Indicating PCM Risk

PCM Risk Albumin g/dl Prealbumin mg/L

Severe <2.5 <100

Moderate 2.6 – 3.2 100 – 170

No Risk >3.5 >170

The health care team or nutrition support team may perform a subjective global assessment (SGA) to assess the patient’s nutritional status. The SGA includes a detailed history and comprehensive physical examination (Gallagher-Allred et al., 1996). The dietary history includes nutritional risk factors, chronic illness (cancer, diabetes, hypertension, renal or liver failure, heart failure, or peptic ulcer disease), trauma, surgery, immobility, socioeconomic problems (finances, inadequate shopping or cooking facilities, elderly living alone, drug or alcohol abuse), adherence to fad diets, presence of dietary allergies, recent changes in diet, ill-fitting dentures, or difficulty chewing or swallowing food (Grant, 1992). Weight loss is reviewed over both a short period (the past 2 weeks) and a longer period (the past 6 months). The clinician obtains a history of gastrointestinal symptoms (nausea, anorexia, vomiting, or diarrhea); decreased or unusual food intake; functional capacity; physical signs of malnutrition (loss of subcutaneous fat, muscle wasting); evidence of fluid retention with edema; and mucosal lesions (glossitis, skin rashes).

The physical examination includes observation of lost subcutaneous fat or muscle wasting; presacral, pretibial, or ankle edema; ascites; abnormal hair; dermatoses; eye diseases; irregular or soft nails; cheilosis; swollen or bleeding gums; and glossitis. Without referring to any labwork or other values, the clinician then derives a “global assessment” of nutritional status. The patient receives an SCA score of A, B, or C (see Table 4). The SCA is a more specific and sensitive method for diagnosing malnutrition than single measurements of albumin, transferrin, delayed cutaneous hypersensitivity, anthropometry, or creatinine-height index (see Tables 5 & 6) (Grant, 1992).

Table 4. Subjective Global Assessment Scores

A = Normal nutritional status

B = Mild malnutrition

C = Severe malnutrition

Table 5.

Nutritional Risk Factors

[] Unplanned weight loss

[] Obesity

[] Diarrhea > 500 cc per day or malabsorption greater than 5 days

[] Excessive vomiting, loss of fluids (via fistulae, open wounds, ostomies, etc.)

[] Catabolic disease states (major trauma, burns, AIDS, DM, renal failure, CHF, etc)

[] Poor oral intake greater than 3 days

[] NPO greater than 3 days

[] Clear or full liquid diet greater than 5 days

[] Dysphagia, odynophagia

[] Patients requiring enteral or parenteral nutrition support

[] Evidence of malnutrition

[] Any condition which interferes with the ability to obtain, ingest, or absorb food

[] Increased metabolic demands

[] Psychological issues (anorexia nervosa, bulimia, eating disorders)

Table 6. Anthropometric Measurements

Used to evaluate the patient’s weight in relationship to ideal

weight and usual weight. The ideal body weight (Hamwi formula) is:

Females = 100 pounds for the first 5 feet of height

+ 5 pounds per inch over 5 feet

Males = 106 pounds for first 5 feet of height

+ 6 pounds per inch over 5 feet

Calculate the Patient’s Energy, Protein, and Calorie Needs

The health care team or nutrition support team calculates the patient’s energy, protein, and calorie needs. Assessment of nutritional status includes measuring total body protein, energy reserves (principally fat), vitamins, minerals, and micronutrients. The clinician must accurately determine energy stores, body protein, and total caloric needs to provide appropriate nutritional support (Torosian, 1995).

Energy. The patient’s basal energy expenditure (BEE) may be calculated using the Harris Benedict Equation (see Table 7). This equation calculates the patient’s resting energy expenditure. The Harris Benedict Equation is multiplied by activity and stress/injury factors to yield estimated total energy calories. More calories are not always better. Complications of overfeeding compromise the patient’s recovery. Isocaloric nutrition support is generally safer, especially when providing total parenteral nutrition (TPN). The physician and dietitian will attempt to achieve a slow, steady weight gain for the malnourished, underweight patient. For example, overfeeding a ventilated patient may cause an increase in carbon dioxide retention and prevent early weaning. Overfeeding also predisposes the patient to hepatic steatosis, carbohydrate intolerance, immunosuppression, suboptimal macronutrient utilization, undesirable fat deposition, increased risk of infection, and unnecessary cost.

Table 7. Harris Benedict Equation

Males: 66.5 + 13.7 (weight in kg) + 5 (height in cm) – 6.7 (age in years)

Females: 655.1 + 9.6 (weight in kg) + 1.8 (height in cm) – 4.7 (age in years)

Average BEE = 25-35 Kcal/Kg BW/d

Protein. Poor nutrition and weight loss are associated with depletion of body protein. The major site of protein loss is skeletal muscle; changes in lean body mass and nitrogen balance reflect changes in muscle protein content. The immune, respiratory, and gastrointestinal systems are also affected by protein deficiency. All metabolic functions of the body (from cell division to obtaining energy from nutrients to host defense mechanisms) are affected by protein deficiency. The role of the other nutrients (fats, carbohydrates, minerals, vitamins) is primarily, although not exclusively, to support protein metabolism. Death will occur when body protein losses approach 30% to 40% (Torosian, 1995).

The current recommended dietary allowance for a healthy adult is 0.6 to 0.8 gm/kg of high-quality protein per day (Ziegler & Filer, 1996). Protein requirements are increased for malnourished adults in the presence of acute illness, but may be restricted with renal or hepatic dysfunction (see Table 8).

Table 8. Protein Requirements for Malnourished Adult Patients

(Measured in gm/kg/day)

No malnutrition; hospitalized 0.8 – 1.0

Mild malnutrition 1.0 – 1.2

Moderate malnutrition or stress 1.2 – 1.5

Severe malnutrition or stress 1.5 – 2.0

Total caloric needs. Total caloric needs increase based on the patient’s activity level and stress level. Activity levels in healthy adults increase the resting energy expenditure by 10% to 20%. Most hospitalized patients have negligible activity levels due to extensive periods of bed rest. However, the hospitalized adult may have significant physiologic stress which is factored into the estimate of total calories (see Table 9). Stress levels are usually no more than 40% above resting energy expenditure, except in extreme cases such as severe burns.

Table 9.

Adjusting Calculated Energy Requirements for Stress

Measured as (Kcal/day)+ BEE x Stress Factor

Medical Diagnosis Stress Factor

Postoperative (no complications) 1.0

Long bone fracture 1.15 – 1.30

Cancer 1.10 – 1.30

Peritonitis/sepsis 1.10 – 1.30

Severe infection/multiple trauma 1.20 – 1.40

Burns (equals approximate BEE + % 1.20 – 2.00

burned BSA)

The health care team or nutrition support team will calculate total caloric needs according to these formulas. However, when a patient’s nutritional and caloric requirements are difficult to assess due to medically complex situations, critical illness, or poor response to treatment, it may be beneficial to determine needs based on indirect calorimetry (metabolic cart) evaluation. Select ICU patients may also be assessed using pulmonary artery catheter values, which generally correlate well with measurements obtained by indirect calorimetry. Valid pulmonary artery catheter caloric calculations depend upon accurate measurement of cardiac output. The formula used is: vO2 (ml/min) 4.83 (Kcal/L) 1.44 = caloric requirements per day (Kimbrough et al., 1997).

The goal of the comprehensive assessment and calculation of nutrient needs is to provide complete nutritional support. If the course of treatment for a hospitalized adult remains uncomplicated, the metabolic and endocrine changes of acute stress or injury will run their course, usually in the first 2 to 7 days. However, if complications arise, the stress response may be continued over extended periods of time and dramatic wasting of body mass will occur. During periods of significant stress as much as 15 to 20 grams of body nitrogen may be lost each day. During acute periods of stress and critical illness, even the most optimal nutrition support will result, at best, in either a 1 to 2 gram positive nitrogen balance per day or just basic maintenance of a neutral nitrogen balance. Every day of delay in initiating appropriate nutritional support may require 7 to 10 days, or more, to “catch up.” If organ failure limits tolerance to nutrition support therapies, it may not even be possible to “hold the line.” Thus, it is essential that nutrition support begins early in the treatment of the critically ill patient. Aggressive nutritional support will minimize marked metabolic losses, possibly shorten recovery time, or at least allow more time for medical and surgical treatments to become effective (Grant, 1992).

Establish the Method of Feeding

The American Society for Parenteral and Enteral Nutrition (ASPEN) has developed a clinical decision algorithm which outlines the selection process for choosing the appropriate nutrition support route (see Figure 3). Major considerations for selecting the enteral versus parenteral feeding route and nutrition support formula include gastrointestinal function, expected duration of nutrition therapy, aspiration risk, and the potential for or the actual development of organ dysfunction.


Enteral. The clinician will compare the associated risk versus benefit of using enteral nutrition or parenteral nutrition. Enteral feedings are always favored when the functional gut is accessible and nutrition support is delivered with skill. When the gut is not functional or usable, parenteral nutrition is a strong second option. Enteral nutrition is indicated for the at-risk patient who will not, should not, or cannot meet nutritional requirements by an oral diet alone. Delivery of nutrition via the gastrointestinal tract is preferred over the parenteral route because it is easier, safer, less expensive, stimulates gut trophic hormones, improves systemic immunity, decreases the incidence of infection, and increases tolerance to septic insult. Mechanical, metabolic, and infectious complications are usually less severe than complications associated with parenteral nutrition. Enteral feedings maintain the structure and functional integrity of the gastrointestinal tract, using nutrients more effectively than if administered parenterally (ASPEN, 1993; Bowers, 1996; Rombeau & Rolandelli, 1997; Torosian, 1995).

Clinicians should consider the many advantages of enteral nutrition over parenteral nutrition (see Table 10). Enteral nutrition therapy is associated with fewer serious complications. Current knowledge about nutritional requirements for nutrients processed through the GI tract is better known than for intravenously administered nutrients. Enteral nutrition can supply gut-specific fuels, glutamine, and short-chain fatty acids; these are absent from commercially available parenteral formulations and help stimulate immune function. Nutrients are needed in the intestinal lumen to maintain the structural and functional integrity of the gastrointestinal tract. Enteral feeding prevents atrophy of intestinal mucosa and the pancreas. It also prevents cholelithiasis by stimulating gallbladder motility. Enteral feedings probably prevent translocation of gut bacteria into the systemic circulation of the critically ill patient, which causes sepsis. Enteral nutrition is less expensive than parenteral nutrition and is often one-tenth the cost. Considering these advantages, if the gut works, use it! (Torosian, 1995).

Table 10.

Benefits of Enteral Feedings

* Promotes nitrogen retention

* Stimulates immune function

* Prevents atrophy of gut mucosa

* Fewer complications

* Less expensive

It is not uncommon for nurses to experience difficulty in administering all of the patient’s nutritional needs enterally due to feeding intolerance. If the gastrointestinal tract possesses adequate absorptive surface and functions sufficiently to absorb some nutrients, it should be used as soon as possible to provide at least a portion of the patient’s nutritional needs. Clinical indicators traditionally used to determine tube feeding tolerance, such as bowel sounds or nasogastric output, are of questionable value for predicting tube feeding tolerance. There is little correlation between bowel sounds and enteral feeding tolerance. The only reliable test of tube-feeding tolerance is a trial period of tube feeding, which should be attempted before committing the patient to parenteral nutrition. During the trial, the nurse will monitor for abnormal abdominal tenderness, distension and firmness, and normal bowel output (see Table 11). Unless a specific contraindication to using the gastrointestinal tract exists, enteral feedings should be attempted as the first line of nutritional therapy (see Table 12) (Bowers, 1996; Torosian, 1995).

Table 11.

Indications for Enteral Feedings

Neurologic and Psychiatric

Cerebrovascular accident



Demyelinating disease

Severe depression

Anorexia nervosa

Failure to thrive

Oropharyngeal and Esophageal





Pancreatitis (mild to moderate)

Inflammatory bowel disease

Small bowel syndrome


Preoperative bowel preparation





Radiation therapy


Organ transplantation

Table 12. Contraindications to Enteral Feedings

[] Inability to safely establish enteral access

[] Intestinal obstruction

[] High-output fistula

[] Intractable vomiting

[] Severe intractable diarrhea Ischemic bowel

[] Known intolerance to enteral feeding

[] Severe malabsorption

[] Patient refusal

Parenteral nutrition. The acutely ill, hospitalized patient who is unable to tolerate enteral feedings should receive parenteral nutrition (PN). Parenteral nutrition is the delivery of nutrients directly into the peripheral or central venous system. Parenteral nutrition is indicated when the gut is nonfunctional; the patient requires bowel rest; or the patient is severely catabolic, with or without pre-existing malnutrition, and the gastrointestinal tract will not be usable within 5 to 7 days (see Table 13). Parenteral nutrition is useful in most cases when enteral feedings are not advisable. For example, PN is indicated for severe gastrointestinal malabsorption, short bowel syndrome, intractable vomiting or diarrhea, severe pancreatitis, paralytic ileus, high-output enterocutaneous fistula, high-dose chemotherapy, radiation, or bone marrow transplantation. PN is sometimes helpful for patients undergoing major surgery with trauma, a history of inadequate oral/enteral diet, 30% to 50% body surface area burns, and inflammatory bowel disease. PN is only considered when it is not possible to feed the patient orally or enterally (see Table 14). PN is expensive and has significant potential for complications (Rombeau & Caldwell, 1993; Torosian, 1995).

Table 13. Indications for Parenteral Nutrition

[] No oral/enteral intake for 5 to 7 days and no intake anticipated for 5 to 7 more days.

[] Severe catabolism and unable to feed orally/enterally for 5 to 7 days.

[] Inadequate gut function that prevents enteral feedings for 5 days or more.

Table 14. Contraindications to Parenteral Nutrition

[] Anticipated treatment less than 5 days.

[] Functional and usable gastrointestinal tract.

[] Inadequate venous access.

[] Patient refusal.

[] Prognosis does not warrant aggressive nutritional support.

Combination therapy. Combining enteral and parenteral nutrition is sometimes in the patient’s best interest. For example, the critically ill patient may tolerate small volumes of enteral feedings while slowly weaning up to the optimal goal rate. Although the patient is receiving minimal nutrients via the GI tract, the trophic feedings prevent gut atrophy. This patient may continue to receive adequate nutrition via TPN for several days until enteral feeding goals are reached. When the patient approaches the enteral goal rate, TPN is weaned off over a period of 1 to 2 hours. If the patient is tolerating enteral feedings well, the risk of rebound hypoglycemia from the discontinued dextrose infusion is minimal.

Select an Access Route for Nutrient Delivery

When selecting an access route for nutrient delivery, always consider the expected duration of therapy and plan of care. Plan ahead!

Enteral devices. Enteral nutrition may be delivered into several areas of the gastrointestinal tract using a wide variety of feeding tubes. Nutrition is delivered directly into the stomach or beyond the pylorus into the small intestine (see Figure 4). The decision to use a specific enteral access device depends on the anticipated duration of nutritional support, aspiration risk, physiology of the GI tract, and preferred placement technique. Feeding tubes may be placed into the stomach, distal duodenum, or proximal jejunum by various techniques including nasoenteric placement, laparotomy, laparoscopy, fluoroscopy, or endoscopy. Nasoenteric tubes are useful for short-term therapy. However, patients who will need nutrition support for more than 4 to 6 weeks will require a long-term feeding device. Each type of feeding tube has specific indications, contraindications, risks, benefits, and implications for nursing care (Bowers, 1996; Campbell & Hall, 1997).


Nasoenteric tubes (NETs) are defined as any enteral feeding device placed through the nose, advanced through the esophagus and beyond. NETs are referred to by the location of the distal tip of the tube,: nasogastric, nasoduodenal, or nasojejunal. NETs are frequently selected for delivery of short-term enteral nutrition because they are easy to place and use. They have a low complication rate and are safe to use for the patient at risk of aspiration when the tip of the feeding tube is placed postpylorically. Small-bore polyurethane or silicone tubes are preferred over large-bore plastic, rubber, or latex tubes. They are more comfortable and less likely to cause nasal irritation, tissue erosion, epistaxis, sinusitis, tracheobronchial injury, or pulmonary compromise (Bowers, 1996).

Nurses place NETs at the bedside, according to hospital policy and procedure. Placement is generally straightforward and uncomplicated. NETs are radiopaque, 22″ to 43″ in length, and may have weighted tungsten tips and/or stiffening stylets to assist with placement. The lubricated tip of the NET is passed through the nares into the nasopharynx and swallowed. Some nurses use a topical local anesthetic, such as viscous lidocaine, to make the insertion more comfortable for the patient. After the tube is placed, proper tip placement is confirmed radiologically and with other techniques. If postpyloric placement into the small intestine is desired, the nurse positions the patient on the right side to take advantage of peristalsis and gravity. The physician may order a prokinetic agent (cisapride, metoclopramide, or erythromycin) to promote transpyloric passage of the NET. The physician may consider fluoroscopic or endoscopic procedures to achieve postpyloric placement in a medically complex patient (Bowers, 1996; Metheny, Reed, Berglund, & Wehrle, 1994).

Enterostomal feeding tubes are placed for patients who will need long-term enteral nutrition. Patients who are comatose, elderly, debilitated, or have esophageal obstruction or facial trauma are good candidates. Enterostomal devices, especially the jejunostomy, are preferred over NETs for neurologically impaired patients because the cardiac sphincter remains intact, decreasing the risk of gastroesophageal reflux and pulmonary aspiration (Bowers, 1996).

The physician places an enterostomal feeding tube by directly accessing the gastrointestinal tract with various surgical, endoscopic, or laparoscopic techniques. The feeding device is placed percutaneously through an artificial stoma created on the abdomen. The device may be temporary or permanent. It is placed into the stomach or small intestine, depending on the patient’s needs. Nurses must be familiar with a wide variety of enterostomal feeding tubes, including the gastrostomy, low-profile gastrostomy (or LPGD), percutaneous endoscopic gastrostomy (PEG), jejunostomy, and dual-access percutaneous endoscopic gastrostomy/jejunostomy (PEJ/G). Care for feeding tubes varies; consult product information booklets that accompany specific devices for instructions on care and maintenance (Bowers, 1996).

Parenteral devices. Parenteral nutrition is delivered via central or peripheral venous circulation, based on the final osmolality of the PN solution and the length of therapy. Peripheral parenteral nutrition (PPN) is administered through a peripheral vein in the upper body. This route of administration is usually effective for temporary supplementation of nutrition when central access is not feasible or when a patient can be partially fed through the gut. Due to the high osmolality of PPN, concentrations of hypertonic components are limited. PPN formulas are not nutritionally complete and are incapable of providing sufficient protein and calories for the acutely or critically ill patient. Proper PPN formulation is essential for successful infusion via peripheral veins. Protein is limited to 3% of total volume or 30 g/L. Dextrose is limited 10% to 12.5% of the total volume. Lipids are administered simultaneously to buffer the PPN solution and protect the peripheral vein from irritation. There are also limitations to the amount of electrolytes and minerals which may be provided peripherally (total K+ not [is greater than] 60 mEq/L). PPN therapy is generally limited to 5 to 7 days because of the high incidence of local inflammation and phlebitis (Kimbrough et al., 1997; Torosian, 1995).

Central venous access must be used for administering TPN. The tip of the central venous catheter (CVC) rests in the superior or inferior vena cava, which affords high blood flow rates and volumes for rapid dilution of the hypertonic TPN solution. Common insertion sites include the subclavian, jugular, basilic, cephalic, and antecubital veins. The femoral insertion site is strongly discouraged because of the high risk of catheter-related infection, difficulty in maintaining a sterile central line dressing, and limitations on patient mobility. CVCs are either percutaneously placed (for short to intermediate-duration TPN) or tunneled (for long-term nutrition support) (see Table 15).

Table 15. Types of Central Venous Catheters


* Groshong

* Hickman

* Implanted vascular ports

* PasPort



* Single lumen

* Multilumen

The health care team or nutrition support team considers the patient’s plan of care when selecting a CVC for TPN therapy. For short-term therapy, a new, single lumen percutaneous CVC dedicated solely to TPN administration is optimal. Multiple lumen CVCs or pulmonary artery catheters increase the risk of catheter infection, even if a new lumen is dedicated to TPN use only. However, in the critically ill patient, multiple lumen CVCs must sometimes be considered due to limited venous access and overall condition of the patient. Tunneled catheters such as the Groshong, Hickman, or implanted port are indicated for patients requiring long-term nutrition support and/or intravenous access. Peripherally inserted central catheters (PICCs) are usually placed by specially trained advanced practice nurses. They can be safely and effectively used for TPN. PICCs offer several advantages over other types of CVCs used for TPN: decreased cost (related to professional charges, placement fees, and device cost); useful for intermediate periods of therapy (up to 6 weeks); low complication rates for infection; and rare incidence of injury to major vessels or surrounding organs (Alhimyary et al., 1996).

The CVC placed for TPN must receive meticulous care including strict aseptic technique. The TPN setup is a sterile, inviolate, closed system. It is not to be used for central venous pressure measurement, administration of medications or blood products, piggyback medications, or blood sampling. Strict aseptic technique is used when accessing the TPN administration setup; connection sites are vigorously cleansed with povidone-iodine or alcohol prior to entering the setup. Total nutrient admixtures (TNA or “3-in-1” TPN) solutions are administered through filtered, non-PVC (DEHP-free) tubing to avoid a toxic interaction between the lipids and plasticizing agents in the tubing. Tubing is changed daily when the new TPN bag is hung; the entire setup expires after 24 hours hang time. All connections must be needleless and Leur-locked to prevent accidental disconnections. TPN is infused via an infusion pump at the prescribed rate. The TPN CVC is regularly inspected, protected with a sterile central line dressing, and cared for according to hospital policies and procedures. The sterile central line dressing is changed regularly and also when it becomes soiled, damp, or nonocclusive. To provide quality care, institutions must develop strict protocols related to the assessment and care of the adult patient receiving TPN (Ryder, 1993; Torosian, 1995)

In 1992, the FDA issued a set of guidelines for CVC insertion, which should be followed for all TPN device placements. Full aseptic technique (maximal barrier setup) at the time of CVC insertion is essential to protect the patient from septic complications. Catheterization is performed with all operators and assistants using proper sterile handwashing, cleansing the skin with a suitable skin antiseptic (povidone-iodine or chlorhexidine), and wearing masks, hats, sterile gowns and gloves, and covering the insertion site with a large sterile drape. Clinicians must be well trained in proper insertion procedures, aseptic technique, and long-term care of the device. Clinicians must be aware of all potential CVC complications, including local infection, sepsis, and mechanical problems (pneumo-/hemo-/hydro-thorax, vessel and cardiac perforation, cardiac tamponade secondary to pericardial effusion, cardiac dysrhythmia, air embolus, catheter malposition, tracheal injury, nerve injury, pulmonary embolus, and sheared catheter). Many of these complications are associated with substantial mortality, although most are avoided or minimized with skilled care. Nurses must be well informed of the appropriate catheter care policies, importance of asepsis, and potential complications in order to provide safe care (Ryder, 1993; Torosian, 1995).

Select a Nutritional Formula

Enteral feeding formulas. There are over 100 commercially prepared enteral formulas available today. Nutritionally complete enteral formulas are available to meet standard or disease-specific needs. Primary considerations in selecting the most appropriate formula are the patient’s protein, carbohydrate, fat, micronutrient, water, and fiber needs. The health care team or nutrition support team has a large variety of products from which to select to best meet the patient’s needs. Formulas are available which are isotonic, fiber-rich, calorie-enhanced, low carbohydrate, elemental low fat, semi-elemental, lactose free, modular, and disease specific.

Disease-specific formulas are designed to meet the altered nutritional and metabolic needs of patients with specific ailments. A wide variety of disease-specific formulas are available for renal, hepatic, critical care, AIDS, malabsorption, hyperglycemia, and pulmonary conditions. For example, a calorie-dense, low-protein product with vitamin and mineral modifications and electrolyte restriction might be chosen for a renal patient. Pulmonary patients with increased CO2 production may benefit from low carbohydrate, moderately high-fat formulas. AIDS patients may benefit from special omega-3 fatty acid-enriched formulas with specialized peptides, fiber, and a disease-specific vitamin and mineral profile. Added MCT oil helps combat lipid malabsorption, which is commonly seen in AIDS. New formulas are being marketed which offer a wide variety of enteral products to meet almost every patient’s needs (Campbell & Hall, 1997).

It is important to consider taste when selecting an enteral formula that may also be taken as an oral supplement. Palatability is influenced by the macronutrients in the formula. Complex nutrients are generally tasty and are well tolerated by most patients. The simple, predigested nutrients in elemental formulas are less palatable. However, elemental formulas can be flavored to improve taste. Elemental formulas are better tolerated by the GI tract than complex nutrient formulas when gut function is compromised. Commercially prepared formulas come in a variety of packaging and delivery systems; all have a long shelf life. If macronutrients need supplementation, modular formulas are available which may be customized (for example, protein powder, oil, fiber).

Parenteral formulas. Parenteral nutrition formulas are tailor-made to meet the patient’s specific nutritional needs. PN comprises macronutrients (protein, carbohydrates, and fats), micronutrients (vitamins, minerals, electrolytes, and trace elements), and fluid. Macronutrients are calculated based on the patient’s nutritional assessment (see Table 16). The protein in PN solutions is provided as amino acids; carbohydrates as hydrolyzed dextrose; and fats as lipid emulsion. The carbohydrate infusion rate should not exceed 6 mg/kg/minute. Lipids are contraindicated for patients with allergy to egg yolk and hypertriglyceridemia (when triglyceride levels are greater than 500 mg/dl). Fat emulsions should not compose more than 40% of the total caloric needs; optimally, less than 30% of calories should come from fat. To prevent an essential fatty acid deficiency (linoleic acid), at least 4% to 10% of total calories should come from fat. Nurses must avoid administering intravenous lipids rapidly and in large amounts because of the direct effect on the reticuloendothelial system, which leads to decreased immune competency. Patients must be watched carefully during the first 30 minutes of the initial infusion of lipids or TNA for an adverse reaction to the lipids (Kimbrough et al., 1997).

Table 16.

Macronutrients in Parenteral Nutrition

Protein (as amino acids)

1 gm = 4 Kcal

Usual dose = 1.0 gm to 1.5 gm/kg/day

Maximum protein concentration for PPN = 3% (30 gm/l)

Carbohydrates (as hydrolyzed dextrose)

1 gm = 3.4 Kcal

Usual dose not to exceed 6 mg/kg/min

Maximum dextrose concentration for PPN = 12.5% (125 gm/l)

if lipids infused simultaneously

Limit PPN dextrose to 10% if not infusing lipids

Fat (as lipids)

1 ml 20% fat emulsion = 2 Kcal

Usual dose not to exceed 40% of total Kcal

Micronutrients and compatible medications are chosen daily based on the patient’s clinical status and laboratory values. The medically unstable patient will need frequent, even daily, TPN micronutrient adjustments based on the clinical situation and frequent laboratory monitoring (see Table 17). Certain medications are compatible with PN and may be added by the pharmacist during the admixture preparation. TPN compatible medications include H2 antagonists, regular insulin, vitamin K, hydrocortisone, and heparin. However, when additive drugs require titration, they must be administered separately from the TPN infusion. It is not possible to titrate infusion rates of drugs added to TPN because of the complications associated with abrupt TPN rate changes (hyper or hypoglycemia, electrolyte imbalances, adverse reaction to rapid infusion of lipids, etc.). No medications should be added to the TPN bag after leaving the pharmacy due to the risk of drug incompatibility and infusate contamination (Kimbrough et al., 1997).

Table 17. Micronutrients for Parenteral Nutrition Daily Adult Recommendations

Trace Elements (3 ml vial)

Chromium (12 mcg)

Copper (1.2 mg)

Manganese (0.3 mg)

Zinc (3 Mg)

Vitamins (MVI-12 adult)

Ascorbic acid (100 mg)

Vitamin A (1 mg or 3,300 IU)

Vitamin D (5 mcg or 200 IU)

Thiamine (B-l) (3 mg)

Riboflavin (B-2) (3.6 mg)

Pyridoxine (B-6) (4 mg)

Niacinamide (40 mg)

Dexpanthenol (15 mg)

Vitamin E (10 mg or 10 IU)

Biotin (60 mcg)

Folic acid (400 mcg)

Vitamin B-12 (5 mcg)

Electrolytes mEq/day

Sodium (60-150)

Phosphate (30-60)

Potassium (60-150)

Chloride (60-150)

Acetate (20-80)

Calcium (9-18)

Magnesium (8-24)

Fluid (30 mg/kg/day or 1500

ml + 20 ml/each additional

kg>20 kg)

Peripheral parenteral nutrition is available in most hospitals and is designed for short-term therapy to bridge the gap until a more optimal form of nutrition support is achieved. It is useful during the initial stages of patient management when diagnostic evaluations preclude adequate oral intake. PPN is not nutritionally complete and does not provide sufficient protein and calories for acutely or critically ill patients. For the infusion to be tolerated by the peripheral veins, PPN has a relatively low caloric density. Lipids may be added to increase caloric density, decrease total PPN volume required, and protect the vein by lowering the solution’s osmolality. The PPN solution must have an osmolality of less than 900 mOsmol/L to prevent thrombophlebitis of the peripheral vein (Ryder, 1993; Torosian, 1995)

Total parenteral nutrition is custom made to meet the patient’s specific needs. TPN is always delivered directly into the central venous system due to the extremely high osmolality of the solution. When a patient is initially started on TPN and/or is medically unstable, the health care team will be very conservative with the use of additives such as electrolytes, insulin, and other agents. Once additives are placed in the PN they cannot be removed; additional requirements may be administered outside the TPN via other intravenousaccess. Otherwise, if the patient’s metabolic picture changes and the additives are no longer needed, the TPN must be discarded. A total nutrient admixture combines the dextrose, amino acids, lipids, and micronutrients into a single, 24-hour bag for infusion. TNA solutions must be carefully inspected for foreign objects, “cracking” or “oiling” (the formation of fat droplets which migrate to the surface of the solution), and “creaming” (the formation of visible layers throughout the PN solution). Foreign objects will be difficult to visualize due to the solution’s opacity. TNA solutions or any PN containing lipids must infuse over 24 hours or less to decrease the risk of fungal infusate contamination.

Establish the Method of Delivery

The health care team or nutrition support team will establish the method of nutrition support delivery based on the patient’s clinical situation, tolerance to feedings, level of activity, plan of care, and discharge plans. Enteral feedings may be delivered by several methods. Continuous feeding uses an enteral feeding pump to control the delivery rate and volume. Continuous feedings are initiated slowly, for example, at 20 to 30 cc/hour for the first 4 to 8 hours using full-strength formula. Feedings into the jejunum are always delivered continuously via pump to avoid distension or rupture of the small intestine. Another delivery system is intermittent feeding, frequently used for gastric feedings. Intermittent feedings may be administered with 100 to 200 cc of full-strength formula by gravity over 15 to 30 minutes every 2 to 3 hours. Intermittent feedings are contraindicated for patients who cannot tolerate large volumes of enteral feedings. A bolus (or gravity drip) feeding is often used for stable patients or at home after discharge. Initiate gravity feedings of full-strength formula at 200 to 300 cc over 15 to 30 minutes every 3 to 4 hours. The bolus method may cause more adverse effects (for example, nausea, cramping, or abdominal distension) than continuous feeding. Bolus feedings should not be used for patients with small bore feeding devices placed in the small bowel. Most formulas are isotonic or semi-hyperosmolar and can be initiated at full strength, eliminating the need to dilute initial feeding formulas (Kimbrough et al., 1997; Ryder, 1993).

Parenteral nutrition is always delivered via an intravenous infusion pump to control the volume and rate. TPN is administered continuously over a 24-hour period or by a cyclic pattern. PPN is delivered continuously via an intravenous pump to maximize the nutritional benefit. A continuous infusion of TPN via pump allows regulation of the patient’s fluid status, serum glucose, and electrolyte levels. Cyclic TPN permits the metabolically stable patient to have a period of free time “off” the infusion pump. Cyclic TPN may be used to encourage oral intake by stimulation of appetite or to prepare the patient for discharge and/or long-term TPN. Prior to initiating cyclic TPN, the health care team will carefully assess the patient’s fluid balance, serum glucose levels, respiratory and cardiovascular status to ensure that the patient will tolerate the entire day’s TPN volume in a 12 to 18-hour period. TPN administration by either method may include a brief initial weaning-up period and a weaning-down period at discontinuation of therapy to allow the pancreas to adjust and to stabilize serum glucose levels. Abrupt cessation of a TPN infusion places the patient at risk for severe rebound hypoglycemia. If TPN must be disconnected emergently (due to a damaged bag or problem with the central venous access device), an infusion of D10W may be temporarily substituted to protect the patient’s serum glucose level (Kimbrough et al., 1997; Ryder, 1993).

Monitor the Patient’s Response to Nutritional Support Therapy

The nurse and members of the health care team will monitor the patient’s response to nutritional support therapy. A variety of clinical indicators will be monitored for the patient receiving enteral nutrition (see Table 18). Weight, vital signs, temperature, fluid volume status, intake and output, clinical signs and symptoms, functional status, laboratory values, and patient response to therapy will be routinely assessed. Baseline and routine labwork includes glucose, clinical chemistry panel (7/60 or 10/60), calcium, magnesium, phosphorus, triglycerides, liver function, CBC, PT, and PTT (Kimbrough et al., 1997).

Table 18. Monitoring Enteral Feeds

* Weights

* I & O

* Blood/urine glucose

* GI function — BMs

* Tube placement

* Positioning

* Gastric residuals

* Rate, strength of formula

* Patient tolerance

* Lab work

The PN patient is carefully monitored to avoid adverse consequences (see Table 19). Routine monitoring includes daily weights, vital signs every 4 to 6 hours, temperature, strict measurement of intake and output, clinical signs and symptoms, labwork and glucose values, functional status, and patient response to therapy. The CVC is carefully observed for symptoms of infection, malfunction, dislodgement, or other complications. Baseline laboratory tests are obtained prior to initiation of PN (10/60, PT, PTT, CBC) and regular labwork (10/60, LFT, CBC, PT, PTT, cholesterol, triglycerides) is obtained weekly and as needed (Kimbrough et al., 1997).

Table 19.

Monitoring TPN

[] Daily weights

[] I & O

[] Blood/urine glucose

[] Administration and setup

[] Central venous catheter and site

[] Complications

[] Temperature, VS’s

[] Lab work


* 10/60

* Calcium

* Magnesium

* Phosphorus

* Triglycerides

* Bili, Alk. phos.


Observe for Possible Complications

Enteral feeding complications. Although enteral feedings are safer than parenteral nutrition, they are not problem-free (see Table 20). Complications include aspiration pneumonia, gastrointestinal, mechanical, and metabolic problems. Other complications include tube migration, fistula formation, clogged feeding tubes, skin excoriation, and nausea/vomiting/diarrhea. Serious complications, such as aspiration pneumonia, may arise when enteral nutrition is provided by untrained health care providers and when monitoring is inadequate (see Tables 21, 22, 23, 24) (Bowers, 1996).

Table 20. Complications of Enteral Feedings

[] Aspiration

[] Mechanical

[] Gastrointestinal

[] Metabolic

[] Refeeding syndrome

Table 21.

Aspiration Risk Factors

[] Altered mental status

[] Gastroesophageal reflux

[] Gastric outlet obstruction

[] Gastroparesis

[] History of aspiration

[] Nasogastric access

* Continuous feeds

* Supine positioning

[] Swallowing dysfunction

Table 22. Mechanical Complications of Enteral Feedings and Associated Factors

Clogged Tube

Inadequate flushing

Inadequately crushed medications

Formula and medication residue

Kinked tube

Highly viscous fiber-rich formula

Tube Displacement

Airway intubation

Coughing or vomiting

Inadvertent dislodgement

Tracheal suctioning



Otitis Media

Large, stiff feeding tube

Excessive pressure on nares

Prolonged placement of NET

Table 23. Gastrointestinal Complications of Enteral Feedings and Associated Factors


Air in tubing

Bacterial contamination of formula

Food allergies

Hyperosmolar feeding formula

Rapid infusion

Medications (antibiotics)

Dumping Syndrome

Cold formula

Rapid feeding


Increased Gastric Residuals

Hyperosmolar formula

Inadequate gastric emptying

Increased feeding rate


Offensive smell

Table 24. Metabolic Complications of Enteral Feedings and Associated Factors


Inadequate free water

Hyperosmolar formula

Electrolyte Imbalance

Formula components

Medical diagnosis


Carbohydrate/insulin imbalance


Medications (steroids)

Hyperosmolar Hyperglycemic

Nonketotic Dehydration

Carbohydrate/insulin imbalance

causing glycosuria, osmotic

diuresis, then dehydration


Excessive fluid administration

Cardiac, hepatic, and/or renal failure

Refeeding Syndrome

Parenteral nutrition complications. The acutely ill patient receiving TPN is at significant risk for mechanical, septic, metabolic, or organ system complications (see Table 25). Mechanical and septic complications are usually related to the venous access device. Metabolic and organ-related complications are related to the nutrient prescription and the patient’s medical condition. Proper catheter placement, safe nursing care using meticulous asepsis, and routine monitoring of clinical status and laboratory values will minimize the occurrence of adverse events (Torosian, 1995).

Table 25. Complications of Parenteral Nutrition

[] Mechanical

[] Septic

[] Metabolic

[] Organ system effects

[] Refeeding syndrome

A myriad of mechanical complications related to central venous access for TPN have been described. They are related to a variety of factors, including the quality of care provided, type of equipment and supplies, and patient’s overall condition; most factors can be controlled to ensure a positive outcome. The TPN CVC must be placed by an experienced physician or PICC nurse because the incidence of mechanical complications greatly increases when unsupervised, inexperienced clinicians place devices (see Table 26). Knowledge of anatomy, asepsis, and potential complications is essential for safe CVC placement. The tip of the CVC should not rest in the heart. CVC position is checked initially and periodically with x-ray. CVCs placed under less than sterile conditions should be removed as soon as possible. Mechanical complications are higher in patients with a previous history of catheter problems, uncooperative patients, and very thin or obese patients (Torosian, 1995).

Table 26. Central Venous Catheters: Mechanical Complications

* Pneumothorax

* Hemothorax

* Chlylothorax

* Hydromediastinum

* Cardiac tamponade

* Tracheal/esophageal injury

* Bleeding

* Arterial injury

* Thrombosis of major vein

* Cardiac arrythmia

* Cardiac perforation

* Endocarditis

* Malpositioned catheter

* Pulmonary embolism

* Air embolism

* Catheter embolism

* Nerve injury

* Thoracic duct laceration

CVC-associated infection or catheter sepsis is a well-known complication of TPN (see Tables 27 & 28). A positive CVC tip culture (preferably using the semiquantitative analysis method) is the generally accepted definition of catheter infection, although catheter tips may be colonized in the absence of clinical signs or positive blood cultures. Some experts suggest that a positive blood culture drawn through the catheter, which grows fivefold more bacterial colonies than a simultaneously drawn peripheral culture, is a more reliable indicator of CVC infection. The CVC infection rate is measured by the number of documented catheter infections either per 100 or 1,000 catheter days (Torosian, 1995).

Table 27. Central Venous Catheter: Infectious Complications

[] Insertion site contamination

* Insertion

* Routine care

[] Catheter contamination

* Insertion

* Breaks into system

* Setup (hub, tubing, stopcocks)

Table 28. Central Venous Catheters: Infectious Complications

[] Infusate contamination

[] Secondary contamination

* Septicemia (bacterial, fungal)

* Infectious process (endocarditis,

osteomyelitis, septic emboli)

[] Concurrent invasive vascular

access contamination

* Hemodialysis

* Swan ganz

* Angiography

CVC sepsis may be caused by bacterial colonization and growth on the inside of the catheter or hub, on the outside of the subcutaneous or intravenous catheter, in the fibrin sleeve, or in the subcutaneous tract. Contamination of the CVC may result from hematogenous seeding (a secondary catheter infection), from skin contamination along the catheter tract, from nonsterile entries into the setup or device, or from contaminated parenteral solutions. When cultured properly, approximately 22% of CVC hubs are contaminated. The risk of a positive CVC tip culture increases as the density of organisms under the CVC dressing increases. In the ICU, other variables that increase the risk of positive tip culture include CVC catheter dwell time greater than 5 days, use of a transparent dressing, and use of the internal jugular or femoral insertion sites. Multilumen CVCs and pulmonary artery catheters have higher infection rates, as do single lumen CVCs which have been violated for uses other than TPN. To minimize the risk of infection, the TPN CVC should be placed using strict aseptic technique; the TPN lumen manipulated as little as possible; careful aseptic technique is used during all routine care; multilumen devices avoided when possible; and sterile, occlusive CVC dressings maintained (Torosian, 1995). CVC sepsis/bacteremia should be considered in the presence of elevated temperature; elevated WBC; elevated blood glucose; localized site erythema, edema, exudate, induration, or tenderness; and shaking chills after flushing the catheter.

Various metabolic complications are associated with the administration of parenteral nutrition (see Table 29). These complications may be related to blood glucose levels, electrolyte abnormalities, lipid tolerance, vitamin deficiency, and essential trace element deficiency. Appropriate nutritional assessment and formula prescription, along with careful patient monitoring, will minimize metabolic complications and allow the health care team to make adjustments as needed. Careful observation should be made of patients who are severely stressed, critically ill, malnourished, have unusual signs and symptoms, or are on long-term TPN (Torosian, 1995).

Table 29. Metabolic: Complications of TPN

* Hyperglycemia

* Hypoglycemia

* Hyperglycemic, hyperosmolar,

nonketotic dehydration

* Diabetes

* Electrolyte imbalance

* Mineral imbalance

* Trace metal deficiency

* Liver function abnormalities

* Fatty acid abnormalities

* Prerenal azotemia

* Hypervolemia, hypovolemia

Organ dysfunction is a fairly common complication of TPN therapy. Liver abnormalities, including elevated SGOT and alkaline phosphatase, steatosis and cholestasis are frequently seen in TPN patients. Gallbladder stasis with sludge or stone formation and intrahepatic cholestasis may be seen after several weeks of TPN. Gut atrophy develops within a few days of intestinal “starvation” and is thought to contribute to translocation of bacteria through a seemingly intact gut to remote sites or to fuel a systemic inflammatory response (multiple system organ failure). These changes can be minimized or prevented by providing very small amounts of enteral feedings, if clinically possible, to minimize gut mucosal atrophy and bacterial overgrowth. TPN also influences pulmonary function in a variety of ways. Severe malnutrition in the critically ill patient leads to increased muscle wasting of the diaphragm and intercostal muscles, which leads to diminished respiratory function, need for prolonged ventilation and pulmonary support, and increased LOS. Respiratory muscle weakness is improved with adequate treatment of severe malnutrition. However, respiratory failure may be precipitated by providing excessive amounts of glucose or inadequate electrolyte (phosphate) supplementation in the TPN (Torosian, 1995).

Avoid Refeeding Syndrome

Refeeding syndrome occurs within 24 to 48 hours after initiating oral, enteral, or parenteral feedings for the severely malnourished patient. It is related to metabolic disturbances, not to the method of feeding (see Table 30). The patient exhibits an increased metabolic rate and significant electrolyte imbalances, especially decreased serum potassium, phosphorus, and magnesium. The nurse initially observes dependent edema and symptoms of fluid overload. Worsening symptoms result in acute congestive heart failure, pulmonary edema, glucose intolerance, lethargy, confusion, weakness, coma, and death. Refeeding syndrome may be avoided by skillful care and careful monitoring of the severely malnourished patient by an experienced health care team.

Table 30. Refeeding Syndrome

[] Potassium

[] Phosphorus

[] Magnesium

[] Fluid (edema)

[] Basal metabolic rate

[] Vitamin flux (water soluble)

[] CHF

[] Pulmonary edema

[] Glucose intolerance

[] Lethargy — confusion

[] Coma — death

Nurse’s Role in Safely Providing Nutrition Support

Nurses must be familiar with every aspect of enteral nutrition support to provide safe care. It is important to understand the normal anatomy and physiology of the gastrointestinal tract, associated pathophysiology, assessment, monitoring, types of enteral formulas and feeding devices, appropriate nursing interventions, and possible complications. Common problems associated with enteral nutrition support are minimized or prevented with good nursing care. For example, the risk of pulmonary aspiration, which is a life-threatening complication, is decreased by properly positioning the patient at a 30 degree angle, using a feeding tube placed beyond the pylorus into the proximal small intestine, and frequently checking gastric residuals. The nurse regularly assesses the patient’s nutritional status, gastrointestinal tolerance, fluid and electrolyte balance, feeding tube function, skin integrity, and functional status. Medications are administered properly to avoid drug-nutrient interactions, adverse medication reactions, or damage to the feeding tube (Bowers, 1996).

Other nursing interventions are directed at accurate delivery of nutrients, proper use of equipment, care and maintenance of the feeding tube, patient teaching, and discharge planning. The nurse observes for potential complications and intervenes in a timely fashion. Comfort measures, oral hygiene, and skin care are provided daily. Emotional support is offered to encourage the patient to participate in self-care, to adjust to changes in body image, and to adhere to the medical plan of care. If the patient is to be discharged with a feeding tube for home enteral nutrition support, education is started early during hospitalization. While providing care, the nurse demonstrates procedures and teaches the patient/family about equipment, formula, administration of feedings, management of complications, and associated rationale. The nurse coordinates home health care arrangements and training of caregivers (Bowers, 1996).

Nurses must have a thorough knowledge of parenteral nutrition support and central venous access to provide safe care. It is important to understand the normal anatomy and physiology of the venous, cardiovascular, and gastrointestinal systems; associated pathophysiology; assessment and monitoring; nursing interventions; and possible complications. The nurse collaborates with members of the health care or nutrition support team to ensure that the patient has no contraindications to parenteral nutrition. The nurse verifies that the patient has an appropriate indication for parenteral nutrition and safe central venous access prior to initiating therapy. Common problems and serious complications associated with parenteral nutrition support can be minimized or prevented with good nursing care. Nursing interventions include assessment, hydration, providing nutrients, proper administration technique; sterile CVC and site care; monitoring for complications; patient education; developing patient-centered goals; and discharge planning. Aseptic technique is essential to safe TPN administration because the patient is at significant risk for infection. Adequate heparinization of the CVC prevents clotting of the lumen when the patient receives cyclic TPN. Sterile CVC site care reduces microorganisms on the skin and helps prevent ascending infection via the catheter tract. Patient education and emotional support allow the patient to understand the care received and adapt to temporary or permanent changes in body image (Ryder, 1993).


How can nurses improve the quality of care provided to malnourished, acutely ill patients? They must become involved in improving the quality of nutritional support for all acutely ill and malnourished adults within their institutions. Working to improve health care delivery systems and communication among all disciplines caring for the malnourished is also essential. If the institution does not have a nutrition support team to provide expert clinical care, the first step is to participate in developing nutrition support clinical pathways or continuous process improvement programs.

The term “clinical pathway” is used frequently, but defining the process and developing new pathways to improve patient care are areas for further growth. Clinical pathways are interventions, ways of tracking interventions, and ways of looking at interventions at certain points in time or during changes in the patient’s clinical condition. The focus of a nutrition support clinical pathway is to achieve patient-centered goals within a prescribed period of time. The intradisciplinary team works together to reduce the LOS and to be financially efficient while simultaneously providing quality patient care. Developing a clinical pathway will assist clinicians to detect variances, including patients who do not achieve goals in a timely fashion (Lykins, Peck, Poole, & Fisher, 1998). A good resource for examples of nutrition support pathways is the American Society for Parenteral and Enteral Nutrition (ASPEN) and the society’s journal, Nutrition in Clinical Practice. Nurses must work together with other health care professionals to develop systems and quality improvement processes which are effective and efficient in terms of providing quality, cost-effective nutritional support to malnourished, acutely ill patients (Mears, 1996).


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