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Total parenteral nutrition in surgical patients.


This independent study offering is designed for nurses and other health care professionals who care for and educate adult surgical patients receiving total parenteral nutrition. 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. Cite common indications for providing total parenteral nutrition.

2. Identify different formulas which can be used to estimate calorie and protein requirements.

3. Define the components of the total parenteral nutrition formula.

4. Describe alterations that must be made in the nutrition plan for patients with selected diseases.

5. List different parameters that can be used to monitor the response to nutrition support.

The metabolic and physiologic response to surgical stress, sepsis, or a severe injury is hypermetabolism. This adaptive response is unspecific and is designed to provide adequate conditions for survival. Hypermetabolism alters normal carbohydrate, fat, and protein metabolism. Malnutrition develops rapidly in hypermetabolic patients affecting end-organ systems and impacting on mortality, recovery time, risk for infection, and wound healing. The magnitude of stress experienced will determine the degree of malnutrition (Chiolero, Revelly, & Tappy, 1997; Cuthbertson, 1942; Souba, 1997). While current nutrition support modalities only have the ability to blunt loss of lean muscle mass, the ability to alter the metabolic response may be in store in the future.

In 1967, Dudrick, Wilmore, and Vars (1967) demonstrated that it was possible for an individual to be fed entirely by venous access using parenteral nutrition formulas. Since this landmark report there have been innumerable advances in providing parenteral nutrition. In this review, indications for using TPN, determination of energy needs, components of the TPN solution, initiation of the solution and monitoring, as well as adjustments made for specific disease states will be discussed.

Indication and Timing of TPN

The indication and timing for initiating total parenteral nutrition (TPN) is controversial. The enteral route is the first choice if the patient has a functional and accessible gastrointestinal tract as it is more physiologic, has fewer complications, and costs less (Lehmann, 1993; Souba, 1997). Common indications for providing TPN include short bowel syndrome, bone marrow transplant, severe acute pancreatitis, gastrointestinal obstruction, and severe pseudomembranous colitis (Sacks & Canada, 1997; Souba, 1997).

In individuals not considered to be at nutritional risk it is reasonable to wait 7 to 10 days prior to initiating specialized nutrition support. On the other hand, patients at high risk benefit from early and aggressive nutrition support (Driscoll & Blackburn, 1990; Lehmann, 1993; Souba, 1997). Surgical patients at risk for poor nutritional outcomes include those with diminished nutrition reserves or requiring extensive preoperative assessment. Identifying patients with an unintentional weight loss prior to admission is the simplest screening mechanism for nutrition risk (Souba, 1997).

The Veterans Affairs Total Parenteral Nutrition Cooperative Study Group (1991) demonstrated a role for providing preoperative TPN in patients requiring major elective surgery. In this prospective randomized trial, 395 patients were grouped according to nutritional status and assigned to either receive TPN or as controls. Severe malnutrition was defined as a serum albumin less than 2.8 gm/dl or a weight loss of 20% and a serum albumin of 3.3 gm/dl. In the severely malnourished group, 7 to 15 days of preoperative TPN significantly decreased the incidence of major noninfectious complications such as anastomotic leak or wound dehiscence. Infectious complications were more frequent in the mildly malnourished patients. The authors recommended preoperative TPN be limited to those classified as being severely malnourished unless there were other indications.

Determining Energy, Protein, Fluid, and Electrolyte Requirements

Optimal nutrition support is patient specific, providing adequate macronutrients and micronutrients on the basis of calculated needs. The goal is to provide nutrients in amounts compatible with the existing metabolic state. Calculation of energy needs is important to minimize use of stored energy reserves. Most simplified formulas will provide an adequate estimate of energy needs (Driscoll, 1990; Quebbeman & Ausman, 1982; Worthington & Wagner, 1989). The formulas in Table 1 were developed based on levels of stress using either weight or body surface area (BSA). Formulas using BSA are more accurate than those based on weight, but as a rule predictive equations underestimate calories in patients with low weights and overestimate needs in the overweight, sedated, or mechanically ventilated (Quebbeman & Ausman, 1982).
Table 1.
Estimating Energy Requirements:
Simplified Formulas

Stress Level                                 Kcal/Kg/Day
Maintenance                                  25-30
Stress or weight gain                        35-40

Body Surface Area (BSA)
Women = 850 x BSA ([m.sup.2]) x 1.2
Men = 900 x BSA ([m.sup.2]) x 1.2

Maintenance protein requirements range from 0.8 to 1.0 gm per kilogram (kg) daily Estimations of protein intake can be adjusted based on evaluation of levels of stress, calorie to nitrogen ratio (Kcal/N+), the results of a 24-hour urine urea nitrogen (UUN) measurement, and the patient's clinical response (Driscoll & Blackburn, 1990; Worthington & Wagner, 1989). Patients sustaining moderate or severe stress may require additional protein. The 24 UUN is useful in calculating protein needs and estimating the level of physiologic stress. Urine urea nitrogen measurement accounts for approximately 80% of estimated protein or nitrogen loss with the remainder occurring via skin and stool. The most efficient ratio of calories to protein that will have a protein sparing effect is reflected in the Kcal/N+ ratio (see Table 2).
Table 2.
Estimating Protein Requirements

                                Kcal/N [+ or -]
Stress Level    Gm/Kg/Day       Ratio
Maintenance     0.8-1.0         125-150:1
Moderate        1.5             100:1
Severe          2.0-2.5         90:1

The intake and output of fluids must be relatively equal to maintain homeostasis (Chenevey, 1987). In patients receiving TPN, the thirst mechanism that helps to regulate fluid intake is bypassed. Therefore, it is necessary to determine daily fluid requirements. An adult requires 30 to 35 ml/kg/day in maintenance fluid intake (Adams & Johnson, 1988; Giner & Curtas, 1986). When calculating the fluid volume for the parenteral nutrition formulation, other fluid sources must be taken into account including additional intravenous fluids, antibiotic, and other medication infusions and appropriate adjustments made. Replacement of acute fluid losses such as those associated with fever, diarrhea stool, or nasogastric tube drainage should be accomplished using a secondary intravenous line. If the patient has stable ongoing exogenous fluid losses, these needs may be met via the TPN.

Daily electrolyte replacement is individualized and will be affected by the patient's primary disease, renal and hepatic function, ongoing losses, and nutritional status (Driscoll, 1990; Giner & Curtas, 1986). The goal is to maintain an adequate urinary output and normal serum electrolyte profile. Table 3 lists the standard range of normal electrolyte requirements, the standard amounts of electrolytes added to a TPN formulation, and the maximum amounts that can be added to the admixture per liter (Adams & Johnson, 1988; Driscoll, 1990).
Table 3.
Daily Electrolyte Needs

Electrolyte     Requirement     Std. TPN     Maximum/Liter
Sodium          60-150          70              102
Potassium       60-150          60               70
Chloride        60-150          70              157
Magnesium        8-24           10              6.7
Calcium         10-15           10              6.7
Phosphorus      30-50 mmol      30               40

Components of the TPN Solution

The TPN formula can be compounded to provide all the macronutrients, fluid, and electrolytes the patient will require over a 24-hour period in one container (Driscoll, 1990; Sacks & Canada, 1997). This type of an admixture is called a 3:1 TPN formula. Benefits of using this type of formulation include more efficient use of the macronutrients, decreased risk for infection, avoiding risks associated with excess carbohydrate calories, and improved cost effectiveness (Andris & Krzywda, 1994; Driscoll, 1990). Components of a standard formula are listed in Table 4.
Table 4.
Standard TPN Formula

70% Dextrose
30% Fat

200 mg/kg/day

35 ml/kg/day

Electrolytes -- Trace
Elements, Vitamins

Sodium chloride         70 mEq
Potassium phosphate     60 mEq
Calcium gluconate       10 mEq
Magnesium sulfate       10 mEq

Macronutrients. The body uses the carbohydrate and fat in the TPN for energy. Carbohydrate is provided as dextrose and is the primary energy source. Glucose is the preferred fuel for the brain, red blood cell, and injured tissue (Lehmann, 1993). These organs require 500 to 700 glucose calories daily to meet their energy needs. Usually 70% of the patient's estimated energy or caloric needs are provided as carbohydrate. The amount of carbohydrate administered to patients with diabetes, stress, chronic obstructive pulmonary disease, and ventilator dependence may need to be limited (Andris & Krzywda, 1994).

The maximum infusion rate for glucose is 5 mg/kg/min and represents the upper limits of the body's ability to metabolize this energy source (Driscoll, 1990; Rosmarin, Wardlaw, & Mirtallo, 1996). If glucose is infused in amounts greater than this, hyperglycemia and fat synthesis occurs with subsequent deposition of fat in the liver. Rosmarin et al. (1996), in a retrospective study of 102 patients receiving TPN, demonstrated the incidence rates for hyperglycemia to be 43% when infusion rates were greater than 5 mg/kg/min as compared to 9% when the rates were less than or equal to 5 mg/kg/min. Carbon dioxide is produced in excessive amounts with overfeeding. The higher rates of carbon dioxide production may stress the surgical patient, compromising respiratory reserve and resulting in carbon dioxide retention (Driscoll & Blackburn, 1990; Murphy & Conforti, 1993).

Fat or lipid is an efficient energy source and is derived from either soybean or safflower oil. Thirty-percent of total calories are typically derived from lipid. A 10% emulsion provides 1.1 Kcal/mL while a 20% emulsion provides 2.0 Kcal/mL. Utilizing lipid as an energy source allows for the provision of fewer carbohydrate calories therefore minimizing the risk of hyperglycemia, carbon dioxide retention, and fatty liver (Driscoll, 1990).

It is necessary to provide 2% to 4% of total calorie needs as fat in order to prevent an essential fatty acid deficiency (EFAD). Essential fatty acid deficiency can occur after 10 days of glucose-based nutrition (Giner & Curtas, 1986). Linoleic and linolenic are the essential fatty acids necessary for cell membrane function and are precursors for prostaglandins. Clinical features of an EFAD are dryness and desquamation of the skin, coarse hair, brittle nails, impaired wound healing, and an increased susceptibility to infection.

Maximum infusion rate for a lipid emulsion is 1.0 to 1.5 gm/kg/day (Driscoll, 1990). Continuous infusion of fat such as occurs when the lipid is a component of the TPN admixture is preferred because there is less fluctuation in the serum triglycerides and oxidation of the fat is more efficient (Sacks & Canada, 1997).

Many drugs are now available in lipid vehicles. These emulsions are equivalent to a 10% lipid emulsion. It is important to monitor their infusion in addition to the parenteral nutrition so as to avoid overfeeding and hypertriglyceridemia (Lowrey, Dunlap, Brown, Dickerson, & Kudsk, 1996). The parenteral formula may need to be altered after consideration has been given to the amount of fat calories received via these infusions.

Protein in the TPN is provided in a crystalline amino acid solution in the form of nitrogen. Amino acids are the building blocks of protein. One gram of nitrogen is equivalent to 6.25 grams of protein. The standard amino acid formulation is a physiologic mixture of essential and nonessential amino acids (Driscoll, 1990; Worthington & Wagner, 1989).

Micronutrients. Parenteral multivitamins are added to the formulation and in general play a role in sustaining metabolic pathways, functioning as co-enzymes to maintain normal cellular function (Andris, 1996). Vitamins also play a vital role in energy transformation, cell renewal, regulation of the immune response, and tissue repair. Vitamin K is not a component of the multivitamin preparation, but can be added separately or given as an intramuscular injection. Vitamin K plays a role in maintaining normal blood coagulation. Therefore, it is not added to the TPN if the patient is receiving anticoagulation. Vitamin K is crucial for converting prothrombin to its active form thrombin. Additional supplements of folic acid, thiamine, and vitamin C or A can also be added.

Trace elements are metabolic co-factors responsible for regulating carbohydrate, fat, and protein utilization (Andris, 1996). They are present in the body in minute amounts as elemental components of metalloenzymes, soluble ionic co-factors, or nonprotein organic molecules. Trace elements routinely added to the TPN are listed in Table 5. Additional supplementation of chromium and zinc in the TPN may be necessary. Chromium plays a role in glucose control by potentiating the action of insulin in peripheral tissues (Andris, 1996). Supplementation with chromium may improve glycemic control in patient's requiring large amounts of insulin or who have a history of diabetes mellitus. In addition to its metabolic functions, zinc also promotes wound healing. Large amounts of zinc can be lost in fluids originating from the gastrointestinal tract. Replacement strategies to restore large losses of zinc have been recommended with patients requiring as much as 17 mg additional zinc daily (Andris, 1996).
Table 5.
Trace Elements

                        Requirement     Std. TPN

Chromium                10-20 mcg        10 mcg
Copper                  300-400 mcg       1 mg
Manganese               0.5 mg          0.5 mg
Zinc                    2.5-4.0 mg        4 mg

Initiating the Parenteral Nutrition Formula

TPN must be administered via a central vein because of the hypertonicity of the solution (Worthington & Wagner, 1989). This allows for the rapid mixing and dilution of the solution. To maintain a constant infusion, TPN solutions are always administered using a mechanical pump. This is done to avoid hyperosmolar nonketotic coma that occurs when glucose is infused too rapidly.

Glucose-based solutions are initiated slowly with the rate gradually increased based on glucose tolerance (Driscoll & Blackburn, 1990; Worthington & Wagner, 1989). These TPN infusions are not to be interrupted or discontinued abruptly without infusing a 10% dextrose solution to prevent rebound hypoglycemia. Mixed fuel solutions using both glucose and fat as an energy source can be infused safely as full nutrition support and stopped abruptly without a tapering schedule. Krzywda et al. (1993) studied the necessity of a tapering protocol for 3:1 formulas by analyzing the time course of plasma glucose concentration after abrupt initiation and discontinuation of TPN. They demonstrated that abrupt start was not associated with severe hyperglycemia nor did abrupt discontinuation result in hypoglycemia.

Nutrition Adjustments for Specific Diseases

The standard TPN formula may need to be adjusted in specific disease states (Andris & Krzywda, 1994). Any single component may be manipulated on the basis of the patient's nutritional status, alterations in metabolism, organ system function, or fluid or electrolyte status.

Renal failure. In acute renal failure there is impaired excretion of creatinine, urea, and other potentially toxic substances resulting in uremia, fluid and electrolyte, and mineral abnormalities. Metabolic alterations that affect nutrition status include glucose intolerance, lipid abnormalities, and alterations in protein and amino acid metabolism (Varella & Utermohlen, 1993). Three primary metabolic disturbances affect the nutrition therapy of patients with acute renal failure: fluid retention, serum electrolyte abnormalities, and increased protein catabolism. The goal in these patients is to maintain or improve nutritional status without worsening uremia or altering fluid and electrolyte balance. In the patient with renal failure, an adequate caloric intake has been associated with improved survival, decrease in rise of blood urea nitrogen, serum phosphorus, and serum potassium levels (Hak & Raasch, 1988).

Patients are given standard calories with a portion of their calories as fat. If fluid restriction is required, additional water is removed and dextrose becomes the sole substrate with fat provided on an intermittent basis to prevent EFAD. Parenteral dextrose in a 70% concentration is more calorically dense than an equivalent volume of 20% lipid emulsion (Driscoll, 1990). Providing protein in standard amounts coupled with the use of dialysis to control azotemia and maintain fluid balance has become the accepted approach in this patient population (Varella & Utermohlen, 1993). Therefore, if the patient is undergoing dialysis, a standard intake of 200 mg of nitrogen per kg per day should be provided. If a patient is not undergoing dialysis, protein must be restricted based on the degree of azotemia to 100 or 150 mg per kg per day. The use of essential amino acids in place of a standard amino acid formulation was originally proposed to be beneficial. However, research has not demonstrated a benefit in terms of improved survival or recovery of renal function (Feinstein, 1988).

Electrolytes are tailored to the patient, but typically restrictions in potassium, phosphorus, and magnesium are required. Patients will require more frequent monitoring of fluid and electrolyte status (Varella & Utermohlen, 1993).

Hepatic failure. The liver is the central metabolic organ and plays a fundamental role in carbohydrate, fat, and protein metabolism. Elevations in serum triglycerides, ammonia levels, and alterations in glucose tolerance in the patient with liver disease reflect alterations in the use of these basic substrates. Providing protein is critical to promote hepatocyte regeneration but may be limited by intolerance (Hiyama & Fischer, 1988). Standard parenteral nutrition formulations can be initiated if the patient is not encephalopathic at baseline (Driscoll & Blackburn, 1990).

Protein allowance is determined on the basis of liver function and clinical response. Monitoring of blood urea nitrogen, serum ammonia levels, and mental status will indicate whether protein should be restricted. Branched-chain amino acid (BCAA) enriched formulas were developed to promote improved protein use and to treat encephalopathy. The use of BCAA-enriched solutions are equal to standard therapy and are not routinely used secondary to their increased cost (Hiyama & Fischer, 1988).

Sodium and water should be limited in patients with ascites. Glucose intolerance and hypertriglyceridemia indicate a need for further alterations in the formulation. If the etiology for the liver disease is alcohol related, increased amounts of thiamine and folic acid can be added to the formulation (Driscoll & Blackburn, 1990).

Cardiopulmonary Failure

Adjustments are made in the nutrition plan when patients have cardiopulmonary failure because the normal mechanism for handling fuel and fluid overload is altered (Murphy & Conforti, 1993). Patients with cardiopulmonary failure should receive fewer total calories (25 calories/kg). The number of calories from fat should be optimized to avoid overfeeding thereby minimizing carbon dioxide production. These patients can receive standard nitrogen. Total volume and sodium intake may need to be limited based on clinical examination to minimize fluid retention. Intake of phosphorus should be optimized to meet the increased cellular energy needs.

Obesity. The initiation of nutrition support should not be delayed in the obese patient (Ireton-Jones & Francis, 1995). A body mass index greater than 27 kg/[m.sup.3] is a commonly used standard for defining obesity. Because commonly used predictive equations will overestimate energy needs in the obese, determining calorie needs should be done using an equation which takes into account the presence of obesity (Quebbeman & Ausman, 1982). Ireton-Jones and Francis (1995) surveyed nutrition support practitioners and confirmed that there was a lack of consensus on how to estimate caloric needs in the obese. The question of whether to use adjusted body weight (ABW) or ideal body weight (IDBW) when calculating energy needs of the obese has been studied (Ireton-Jones & Turner, 1991). Ireton-Jones and Turner (1991) determined that ABW could be used in predictive equations based on the results of a regression analysis correlating ABW with measured energy expenditures.

Hypocaloric feeding has been recommended in the obese. Studies evaluating the safety and efficacy of hypocaloric nutrition regimens in the acutely ill obese have demonstrated an ability to achieve positive nitrogen balance and heal wounds (Burge, Goon, & Choban, 1994; Choban, Burge, & Flancbaum, 1997; Dickerson, Rosato, & Mullen, 1986). Approximately half the estimated calorie needs are provided solely from glucose. A typical hypocaloric formula designed for an obese patient may provide 800 calories. Lipids are provided on a limited basis to meet EFA needs. Providing protein is a priority with patients typically receiving two grams of protein per kilogram body weight.

Chronic malnutrition. Special care is required when initiating nutrition support in a chronically malnourished patient. When these patients receive concentrated calories via the intravenous route, alterations may be seen in fluid and electrolyte balance, glucose metabolism, and vitamin levels (Heymsfield, Casper, & Funfar, 1987). A refeeding syndrome resembling congestive heart failure has been identified and is associated with aggressive early nutrition support in this group of patients (Solomon & Kirby, 1990). With refeeding there is a rapid increase in extracellular fluid due to the antidiuretic effect of carbohydrate. This results in fluid retention and overload in a patient with limited cardiac and pulmonary reserve. As the body is supplied with calories, there is an associated increase in the basal metabolic rate and oxygen consumption compounding the stress on the cardiopulmonary system.

Patients with severe malnutrition or starvation are depleted in total body phosphorus, potassium, and magnesium (Heymsfield et al., 1987). Serum values may be normal, but with the infusion of dextrose and conversion to an anabolic state, these components are shifted rapidly into the intracellular space. This shift of electrolytes into the cell may precipitate dangerously low serum values.

Therefore, the following alterations are made in the nutrition plan (Heymsfield et al., 1987). Initially, standard calories are provided and fluid volume and sodium intake is restricted. After 5 to 7 days of nutrition support, maximal weight gain secondary to fluid retention will have occurred, signaling the ability to increase calories to a level which will result in repletion of lean body mass (35-40 Kcal/kg). From the start, additional protein is provided with patients receiving 225-250 mg/kg/day of nitrogen. Increased amounts of phosphorus, magnesium, and potassium may be required due to the synthesis of lean tissue and the return to the intracellular space of these electrolytes and minerals. Vitamins should be administered routinely. These individuals are susceptible to thiamine deficiency and may require additional supplementation.

Assessing and Monitoring Response to Nutrition Support

Routine monitoring. Monitoring intake and output along with daily weights allows for assessment of hydration status. The importance of accurate repetitive measurements of body weight cannot be overemphasized. In the surgical patient, changes in weight must be interpreted in view of other clinical and laboratory information (Adams & Johnson, 1988). Weight gain greater than 1 kg a week reflects positive fluid balance and not accrual of lean body mass (Souba, 1997). Expected urinary output in the adult is 1,500 [+ or -] 500 ml per day. The clinical signs of hydration that should be monitored include thirst, skin turgor, edema, heart rate, and orthostatic blood pressure changes.

A fingerstick to monitor glucose should be performed on all patients for the first 24 hours. If the values are normal then there is no need to continue monitoring (Driscoll, 1990; Worthington & Wagner, 1989). In patients at risk for hyperglycemia (for example, experiencing diabetes mellitus, pancreatitis, or infection), fingerstick glucose monitoring may be required for a longer period of time.

Routine laboratory studies should include a chemistry profile, serum triglyceride measurement, calcium, phosphorus, and magnesium values (Giner & Curtas, 1986). Most institutions will have a standardized routine for monitoring laboratory studies. Patients with excessive gastrointestinal losses due to pancreatic fistulas, small bowel fistulas, or short bowel syndrome are at risk for a zinc deficiency and should have serial zinc determinations (Andris, 1996).

Assessing nutrition response. There is no routine laboratory test specific for monitoring nutrition status. The relevance and reliability of current methods remain controversial (Hill & Windsor, 1995). Clinical assessment may be as effective as objective measures (Souba, 1997). Because nutrition is a major factor affecting protein synthesis, clinicians have found that a measurement of several circulating proteins can be a useful adjunct to the clinical evaluation. The relatively rapid turnover and short half-life of albumin and transferrin make them sensitive indicators of change in nutrition status (Gianino & St. John, 1993) Although these tests may be useful, they are affected by other variables such as hydration status and the liver's ability to synthesize protein.

Serum albumin is the most commonly measured visceral protein (Gianino & St. John, 1993). It has a half-life of 20 days. Serum levels of albumin slowly fall and recover in response to changes related to nutrition status. The stress of surgery or illness alone can decrease albumin levels. Acute changes in albumin concentration may be a more accurate reflection of hydration status. Transferrin is a serum protein that aids in the transport of iron. It has a half-life of 8 days and may be a more sensitive indicator of the patient's response to nutrition interventions (Gianino & St. John). Iron deficiency and, infection can alter transferrin levels.

Nitrogen balance determinations are a frequently used indicator of response to nutrition therapy and reflect an approximation of protein and energy balance (Gianino & St. John, 1993), Positive nitrogen balance reflects an anabolic state, while a negative nitrogen balance reflects a catabolic state. Nitrogen balance can be estimated using the following formula: nitrogen balance = 24 hour nitrogen intake - (24 hour UUN + 4 Gm) (Gianino & St. John, 1993). The addition of four grams to the 24 UUN accounts for an estimate of unmeasured nitrogen losses in the stool and sweat. The significance of visceral protein measurements must be assessed in conjunction with the patient's clinical response and nitrogen balance determinations.


The goals of nutrition support in the surgical patient are to meet energy needs, prevent protein catabolism, and promote protein anabolism through the provision of adequate substrate. Stressed patients require adequate nutrition to blunt the catabolic response, wasting of lean body mass, impairment of organ function, immune dysfunction, and to promote wound healing.


Adams, M.B., & Johnson, C. P. (1988). Fluid and electrolyte therapy. In R.E. Condon, & L.M. Nyhus (Eds.), Manual of surgical therapeutics (pp. 163-185). Boston: Little, Brown, & Company.

Andris, D.A. (1996). Substrate metabolism: Vitamins, minerals, trace elements. In K.A. Hennessy, & M.E. Orr (Eds.), Nutrition support nursing core curriculum (pp. 4-14, 17). Silver Spring, MD: American Society for Parenteral and Enteral Nutrition.

Andris, D.A., & Krzywda, E. A. (1994). Nutrition support in specific diseases: Back to basics. Nutrition in Clinical Practice, 9, 28-32.

Burge, J.C., Goon, A., & Choban, P.S. (1994). Efficacy of hypocaloric total parenteral nutrition in hospitalized obese patients: A prospective, double-blind randomized trial. Journal of Parenteral and Enteral Nutrition, 18, 203-207.

Chenevey, B. (1987). Overview of fluids and electrolytes. Nursing Clinics of North America, 22(4), 749-759.

Chiolero, R., Revelly, J.P., & Tappy, L. (1997). Energy metabolism in sepsis and injury. Nutrition, 13(9), 45-51.

Choban, P.S., Burge, J.C., & Flancbaum, L. (1997). Nutrition support of obese hospitalized patients. Nutrition in Clinical Practice, 12, 149-154.

Cuthbertson, D.P. (1942). Post-shock metabolic response. Lancet, 433-436.

Dickerson, R.N., Rosato, E.F., & Mullen, J.L. (1986). Net protein anabolism with hypocaloric parenteral nutrition in obese stressed patients. American Journal of Clinical Nutrition, 44, 747-755.

Driscoll, D.F. (1990). Clinical issues regarding the use of total nutrient admixtures. Annals of Pharmacotherapy, 24, 296-301.

Driscoll, D.F., & Blackburn, G.L. (1990). Total parenteral nutrition 1990: A review of its current status in hospitalized patients, and the need for patient-specific feeding. Drugs, 40(3), 346-363.

Dudrick, S.J., Wilmore, D.W., & Vars, H.M. (1967). Long-term total parenteral nutrition with growth in puppies and positive nitrogen balance in patients. Surgical Forum, 18, 356-357.

Feinstein, E.I. (1988). Total parenteral nutritional support of patients with acute renal failure. Nutrition in Clinical Practice, 3, 9-13.

Gianino, S., & St. John, R.E. (1993). Nutritional assessment of the patient in the intensive care unit. Critical Care Nursing Clinics of North America, 5(1), 1-16.

Giner, M., & Curtas, S. (1986). Adverse metabolic consequences of nutritional support: Macronutrients. Surgical Clinics of North America, 66(5), 1025-1047.

Hak, L.J., & Raasch, R.H. (1988). Use of amino acids in patients with acute renal failure. Nutrition in Clinical Practice, 3, 19-22.

Heymsfield, S.B., Casper, K., & Funfar, J. (1987). Physiologic response and clinical implications of nutrition support. American Journal of Cardiology, 60, 75-81.

Hill, G.L., & Windsor, J.A. (1995). Nutritional assessment in clinical practice. Nutrition, 11(2), 198-201.

Hiyama, D.T., & Fischer, J.E. (1988). Nutritional support in hepatic failure. Nutrition in Clinical Practice, 3, 96-105.

Ireton-Jones, C.S., & Francis, C. (1995). Obesity: Nutrition support practice and application to critical care. Nutrition in Clinical Practice, 10, 144-149.

Ireton-Jones, C.S., & Turner, W.W. (1991). Actual or ideal body weight: Which should be used to predict energy expenditure? Journal of the American Dietetic Association, 91, 193-195.

Krzywda, E.A., Andris, D.A., Whipple, J.K., Street, C.C., Ausman, R.K., Schulte, W.J., & Quebbeman, E.J. (1993). Glucose response to abrupt initiation and discontinuation of total parenteral nutrition. Journal of Parenteral and Enteral Nutrition 17(1), 64-67.

Lehmann, S. (1993). Nutritional support in the hypermetabolic patient. Critical Care Nursing Clinics of North America, 5(1), 97-106.

Lowrey, T.S., Dunlap, A.W., Brown, R.O., Dickerson, R.N., & Kudsk, K.A. (1996). Pharmacologic influence on nutrition support therapy: Use of propofol in a patient receiving combined enteral and parenteral nutrition support. Nutrition in Clinical Practice, 11, 147-149.

Murphy, L.M. & Conforti, C.G. (1993). Nutritional support of the cardiopulmonary patient. Critical Care Nursing Clinics of North America, 5(1), 57-64.

Quebbeman, E.J., & Ausman, R.K. (1982). Estimating energy requirements in patients receiving parenteral nutrition. Archives of Surgery, 117, 1281-1284.

Rosmarin, D.K., Wardlaw, G.W., & Mirtallo, J. (1996). Hyperglycemia associated with high, continuous infusion rates of total parenteral nutrition dextrose. Nutrition in Clinical Practice, 11, 151-156.

Sacks, G.S., & Canada, T. (1997). New strategies in specialized nutrition support. Hospital Pharmacist Report, 42-51.

Solomon, S.M., & Kirby, D.F. (1990). The refeeding syndrome: A review. Journal of Parenteral and Enteral Nutrition, 14(1), 90-97.

Souba, W.J. (1997). Nutritional support. The New England Journal of Medicine, 336(1), 41-48.

Varella, L., & Utermohlen, V. (1993). Nutritional support for the patient with renal failure. Critical Care Nursing Clinics of North America, 5(1), 79-96.

Veterans Affairs Total Parenteral Nutrition Cooperative Study Group. (1991). Perioperative total parenteral nutrition in surgical patients. The New England Journal of Medicine, 325(8), 525-532.

Worthington, P.H., & Wagner, B.A. (1989). Total parenteral nutrition. Nursing Clinics of North America, 24(2), 355-371.

Deborah A. Andris, BSN, RN, CNSN, is Nutrition Support Nurse, Department of Surgery, Medical College of Wisconsin, Milwaukee, WS.
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Title Annotation:includes continuing education posttest
Author:Andris, Deborah A.
Publication:MedSurg Nursing
Date:Apr 1, 1998
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