Current uses of total parenteral nutrition

Current uses of total parenteral nutrition

Michael M. Meguid

Total parenteral nutrition provides intravenous carbohydrates in the form of glucose, protein in the form of amino acids, lipids in the form of triglycerides, and vitamins, minerals and trace elements. The primary indication for its use is therapy for the patient who cannot eat, should not eat, will not eat or cannot eat enough. When given in amounts necessary to meet a patient’s metabolic needs, this therapy is generally referred to as total parenteral nutrition; when given in amounts exceeding metabolic needs, it is called hyperalimentation.

Before the availability of lipid emulsions, glucose-based parenteral nutrients were generally administered through a central vein, most commonly the subclavian vein, to prevent chemical thrombophlebitis caused by the high osmolality of the infusion. Iso-osmotic lipid emulsions allow parenteral nutrients to be given as a mixed-fuel solution in which the three macronutrients–glucose, lipids and amino acids–and the micronutrients are mixed together (total parenteral admixture or TPA) in a single delivery system that more closely resembles a physiologic situation.[1] A hypertonic, glucose-based nutrient system, in which lipids are given twice weekly via piggyback infusion, however, is still used to deliver parenteral nutrition.

Despite widespread application of total parenteral nutrition during the past two decades, it is commonly accepted today that it should be used only in situations where nutritional support has been proved efficacious.[2]

Effects of Malnutrition

The relationship between preoperative weight loss and postoperative mortality in patients undergoing operation for benign peptic ulcer disease was first reported in the early 1930s. Patients with a preoperative weight loss of more than 20 percent had a postoperative mortality rate of 33.3 percent, versus a 3.5 percent rate in patients with a smaller amount of weight loss. In the mid-1930s and early 1940s, hypoproteinemia was documented as a cause of delayed gastric emptying and prolonged ileus, an increased incidence of wound dehiscence, delayed bone callus formation and an increased risk of infection.

These early observations were extended to show that postoperative complications were more frequent in hypoproteinemic surgical patients, that malnourished burned children had an increased risk of sepsis and that hemorrhagic shock was not as well tolerated by patients in a state of protein depletion as by well-nourished control subjects. Thus, similar results were obtained in a variety of situations and with different physiologic insults, leading to the common conclusion that complications are more likely to occur in poorly nourished patients. More recent studies have once again demonstrated this association in a variety of clinical settings.[3]

The mechanisms by which malnourished patients are more prone to postoperative complications are often synergistic. Mechanical breakdown of the skin and mucosal barriers by surgical incision and manipulation leads to unavoidable contamination by microorganisms. Consequently, a normal host defense mechanism is essential to prevent septic complications. Impaired immunologic functions accompanying the malnourished state include reduced cell-mediated immunity and inflammatory response, with decreases in humoral or antibody components (B lymphocytes), cell-mediated components (T lymphocytes), phagocytic components (polymorphonuclear neutrophils, macrophages and the reticuloendothelial system) and complement (direct or alternate pathway). The consequence of this impaired immunologic state is an increased susceptibility to postoperative infection.[4]

Malnutrition affects the resumption of gastrointestinal tract function after surgery; a considerable delay occurs in the malnourished patient relative to the well-nourished patient.[5] Malnutrition also affects skeletal muscle function. Muscle bulk and muscle metabolism are reduced; this reduction is the most recognizable aspect of gross malnutrition. Impairment of the respiratory muscles leads to reduction of both vital capacity and resting minute ventilation. Moderate starvation alone has been shown to cause a significantly impaired hypoxic ventilatory response. Cardiac mass and contractility are reduced.

Renal function may be impaired from a fall in glomerular filtration rate secondary to the malnutrition-related decrease in circulatory volume. Fibroplasia is also reduced in malnourished patients, with a resultant delay in wound healing.

Starvation decreases brain neurotransmitters, leading to a state of apathy, with a diminished sense of self-motivation. Since malnutrition has a deleterious effect on every major system in the body, it is not surprising that morbidity and mortality increase in malnourished patients following surgical trauma or hospitalization for medical conditions.[3]

Clinical Settings

The paramount use of total parenteral nutrition should be to prevent or correct malnutrition that occurs secondary to a disease state or therapy. The definition and quantification of malnutrition have recently been reviewed[3,6,7] and will not be discussed in this article. However, it is important to emphasize that the presence of malnutrition or the anticipation that a patient’s nutritional status will deteriorate should form the basis for a clinical decision to start total parenteral nutrition, independent of the patient’s underlying disease or required treatment. The clinical settings in which total parenteral nutrition is currently accepted are summarized in Table 1.

SHORT-BOWEL SYNDROME

Short-bowel syndrome probably represents the best example of the impact of total parenteral nutrition on a life-threatening disease state.[8] Survival on oral intake is precluded if less than 2 feet of intestine remain beyond the duodenum. Before the availability of parenteral nutrition, patients undergoing extensive resection of the small intestine because of infarction, trauma, Crohn’s disease, radiation enteritis or neoplasia inevitably died because of their inability to absorb nutrients.

Total parenteral nutrition ensures survival, and a relatively normal life, in patients with short-bowel syndrome. It also assists the residual intestine to undergo adaptive changes–small bowel dilatation, villous enlargement, epithelial hyperplasia and enhanced absorption–that eventually permit subsequent use of the gastrointestinal tract for a home enteral nutrition program.

PERIOPERATIVE

Preoperative. The rationale for preoperative use of total parenteral nutrition is based on the evidence that 40 to 70 percent of patients undergoing surgery for malignant or nonmalignant disease of the gastrointestinal tract are malnourished.[9-11] Randomized studies have been performed to clarify whether preoperative total parenteral nutrition is effective in reducing postoperative morbidity and mortality.[10,12-16] From these studies, it can be concluded that two to three days of total parenteral nutrition before surgery does not improve surgical outcome. An improvement in outcome is seen only after five to seven days of total parenteral nutrition. A statistically significant reduction in major postoperative complications and mortality is achieved when total parenteral nutrition is given for at least seven to 10 days before surgery.[3]

Postoperative. After surgery, patients generally enter a period of poor or inadequate oral intake. The decision to provide total parenteral nutrition for supportive purposes immediately following surgery, in the absence of conclusive data,[17-19] is based on clinical judgment. Most patients with adequate preoperative nutrition are able to tolerate a limited postoperative period (three to five days) without nutrient intake. The malnourished patient, however, is unable to withstand this type of controlled starvation, particularly if a complication arises.

INFLAMMATORY BOWEL DISEASE

A high incidence of malnutrition has been reported in patients with inflammatory bowel disease. The frequency of acute malnutrition is 33 to 48 percent in Crohn’s disease and 58 to 72 percent in ulcerative Colitis.[20,21] Chronic malnutrition, however, is more common in Crohn’s disease because the small bowel is often affected, whereas ulcerative colitis affects the colon.

Despite the high frequency of malnutrition in this situation, the primary role of nutritional support (total parenteral or enteral nutrition) in influencing the outcome of inflammatory bowel disease remains largely unclear. Uncontrolled clinical studies during the past 15 years have shown that in-hospital remission of ulcerative colitis in patients receiving total parenteral nutrition ranges from 9 to 100 percent, while long-term remission is 60 percent. For Crohn’s disease, in-hospital remission has varied from 23 to 100 percent; long-term remission has been 69 percent.[22] In inflammatory bowel disease, total parenteral nutrition is used primarily to prevent or reverse malnutrition and its associated complications.

Results from prospective trials evaluating the efficacy of total parenteral nutrition as compared with other treatments for ulcerative colitis and Crohn’s disease are inconclusive. In one study, total parenteral nutrition as an adjunct to prednisone was as effective as prednisone alone in patients with ulcerative colitis.[23] In another study, patients receiving steroids for colitis due to Crohn’s disease or ulcerative colitis localized to the colon had a remission rate comparable to that in patients treated with total parenteral nutrition or maintained on an oral diet.[24] However, the response to parenteral nutrition and bowel rest was found to be significantly higher in patients with Crohn’s disease than in patients with ulcerative colitis. In a study of patients with long-standing Crohn’s disease who were maintained solely on total parenteral nutrition for a prolonged period, parenteral nutrition was not a valid alternative to surgery in the treatment of the complications of Crohn’s disease.[25] Similarly, recent randomized studies[26,27] led to the conclusion that bowel rest achieved with total parenteral nutrition does not significantly influence remission or long-term outcome in patients with Crohn’s disease.

ENTEROCUTANEOUS FISTULAS

Enterocutaneous fistula is associated with high morbidity and a lengthy hospitalization. Malnutrition occurs in 53 percent of patients with gastric or duodenal fistulas, 74 percent with jejunal or ileal fistulas and 20 percent with large bowel fistulas. Studies have demonstrated overall mortality rates (with and without definitive therapy) of 62 percent for gastric or duodenal fistulas, 59 percent for jejunal or ileal fistulas and 64 percent for large bowel fistulas.[28]

The indications for total parenteral nutrition in patients with enterocutaneous fistulas are the high risk of malnutrition and the need for bowel rest to decrease intestinal secretion and fistula drainage, resulting in earlier closure. In the absence of prospective randomized trials to evaluate the therapeutic effects of total parenteral nutrition on the clinical outcome of patients with enterocutaneous fistulas, the current view is that the role of total parenteral nutrition is primarily supportive, to treat malnutrition, to prevent further deterioration of the nutritional state and to decrease the incidence of postoperative complications in patients who eventually need surgery. Somatostatin (Reducin), a potent inhibitor of intestinal secretions, has dramatically improved the outcome for patients with enterocutaneous fistula by promoting spontaneous closure.[29]

PANCREATITIS

The role played by the pancreas in the digestive process is so crucial that acute or chronic failure of this organ results in rapid deterioration of the nutritional state. Furthermore, acute pancreatitis is accompanied by severe catabolic stress and increased metabolic demand, and many patients with pancreatic disease are alcoholics who already have underlying malnutrition. Based on recent uncontrolled and prospective studies of the efficacy of total parenteral nutrition in reversing pancreatic disorders,[30,31] total parenteral nutrition, although not curative, appears to be of benefit in cases of severe necrotizing pancreatitis.[32] It is also useful following complications such as fistulas, pseudocysts or pancreatic ascites. Although still debated, evidence indicates that the use of lipid solutions is well tolerated in patients with pancreatitis, even in the presence of hyperlipidemia.[31,33]

CANCER

Malnutrition is frequent in cancer patients. It is usually caused by anorexia. A series of metabolic alterations that lead to a catabolic state contribute further to malnutrition, which adversely influences patient outcome. In addition, adjuvant medical, surgical and radiation treatments tend to aggravate malnutrition.

Despite numerous randomized prospective studies of the effect of total parenteral nutrition on the outcome of cancer patients, it should be emphasized that total parenteral nutrition is not a treatment for cancer itself. Data clearly indicate that total parenteral nutrition is effective for preventing or treating the malnutrition that accompanies neoplastic disease or results f rom antitumor therapy.

Currently, total parenteral nutrition is used as an adjunct to antineoplastic therapy and for supportive care if it is expected that treatment will produce or worsen malnutrition. Some studies have shown that total parenteral nutrition increases tolerance and/or response to chemotherapy,[34] radiation therapy[35] and surgery.[36] However, recent reports suggest that its use in cancer patients with a good or only mildly deteriorated nutritional state who have surgery, radiation therapy or chemotherapy is of no benefit and may be associated with a higher incidence of infection.[16]

Whether total parenteral nutrition stimulates tumor growth is a question that remains unanswered.[37] The general consensus is that in the absence of total parenteral nutrition, the tumor, which has an autonomous metabolism, continues to grow. Total parenteral nutrition merely ensures that the host remains nutritionally replete. Further studies are needed to determine if total parenteral nutrition, in combination with antitumor therapy, may significantly influence therapeutic response and general outcome, as suggested by some studies.[19]

BONE MARROW TRANSPLANTATION

Bone marrow transplantation has serious nutritional consequences, including anorexia, nausea, vomiting, diarrhea, malabsorption, negative nitrogen balance and weight loss. These nutritional disabilities result from pretransplant chemotherapy and radiation therapy used in cytoreduction treatment and from post-transplant complications such as infection and graft-versus-host disease. As a result, at least 50 percent of patients undergoing bone marrow transplantation have malnutrition.[38]

The debilitated condition of the gastrointestinal tract predisposes these patients to viral, bacterial and fungal infections of the bowel, which lead to further mucosal damage and malabsorption. Increased nitrogen loss is compounded by relative immobilization, infection and graft-versus-host disease.[39]

Because of the unreliability of the enteral route in these patients, total parenteral nutrition has become routine.[40] Early nutritional support is important in bone marrow transplantation, because patients show a loss of lean body tissue during the first few weeks after the transplantation.

Providing total parenteral nutrition to well-nourished bone marrow transplant recipients enhances survival, diminishes relapse and shortens the post-transplant hospital stay.[41] Total parenteral nutrition, however, does not influence engraftment, duration of overall hospitalization and the occurrence of acute and chronic graft-versus-host disease or bacteremia. Thus, total parenteral nutrition has a positive effect on long-term outcome. Total parenteral nutrition is indicated even for well-nourished individuals during the cytoreduction process and bone marrow transplantation.

CARDIAC SURGERY

Cardiac glycogen levels are an indicator of myocardial nutrition status. Increasing cardiac glycogen concentration through intravenous glucose and fat loading in the immediate preoperative period favorably affects cardiac glycogen levels.[42] Providing total parenteral nutrition overnight before coronary artery bypass surgery increases the myocardial glycogen concentration, resulting in fewer severe postoperative ventricular arrhythmias, less vasopressor dependency, fewer transmural myocardial infarctions and greater postoperative survival.[43]

OBSTETRICS

Two percent of all patients receiving total parenteral nutrition are women with obstetric problems.[44] Total parenteral nutrition is used in pregnancy for two main reasons: (1) to provide adequate nutrition for a woman with prolonged, severe hyperemesis gravidarum and (2) when there is diminished absorption or assimilation of adequate nutrients secondary to exacerbation of preexisting illnesses, such as inflammatory bowel disease and recurrent pancreatitis.

Total parenteral nutrition is used primarily in the second half of pregnancy and is usually discontinued well before delivery. An appropriately sized infant is delivered in 61 percent of patients who require total parenteral nutrition. It is believed that many infants who are small for gestational age at birth were already growth-retarded before total parenteral nutrition was initiated.

ACUTE RENAL FAILURE

A sudden hypercatabolic decrease of renal function, with serum creatinine levels greater than 3 mg per dL (260 [Mu]mol per L) for two or more days following surgery, major trauma or multiple organ failure, is fatal in about 50 percent of patients.[45] Protein and calorie requirements in patients with acute renal failure are significantly increased[46] and are further increased by frequent dialysis. The survival rate in acute renal failure correlates significantly with adequate caloric intake.[45] Total parenteral nutrition markedly contributes to improved outcome in patients with acute renal failure.

Unconfirmed is a claim that patients with acute renal failure benefit from parenteral formulas containing a mixture of eight essential amino acids, which would allow better nitrogen utilization and decreased urea production.[47] Although based on a very solid rationale, this theory has not been confirmed in randomized controlled trials.[48]

HEPATIC FAILURE AND ENCEPHALOPATHY

The aim of nutritional support in patients with chronic hepatic failure should be to correct or prevent malnutrition without worsening–or even improving–the metabolic effects of advanced liver disease. Metabolic effects include hyperaldosteronism with reduced tolerance to sodium and water, impaired tolerance to carbohydrates, elevated muscular protein breakdown and reduced tolerance to protein loads with pending or overt hepatic encephalopathy.

These metabolic changes make the nutritional approach to the treatment of chronic liver failure extremely complex. Fluid overload should be prevented by the infusion of hypertonic glucose; exogenous insulin is recommended to promote peripheral glucose assimilation and to prevent hyperglycemia. Lipid solutions, which provide high amounts of calories in a smaller volume, have been discouraged because of the inability of cirrhotic patients to adequately metabolize exogenous fat. However, plasma clearance of exogenous triglycerides in the amounts currently administered in total parenteral formulas has been shown in both compensated[49] and decompensated cirrhotic patients[50] to be similar to that found in normal subjects.

The characteristic plasma amino acid profile seen in patients with cirrhosis–high aromatic and low branched-chain amino acid (BCAA) levels–is involved in the pathogenesis of hepatic encephalopathy.[51] The ability of BCAA-enriched solutions to normalize the plasma amino acid pattern in chronic liver failure[52] and to reverse hepatic encephalopathy has been shown in several studies[53,54] but has not been accepted unequivocally. Strong support for the efficacy of BCAA-enriched total parenteral nutrition in the treatment of hepatic encephalopathy is based on data from nine controlled clinical trials.[55]

ACQUIRED IMMUNODEFICIENCY SYNDROME

Malnutrition is common in patients with acquired immunodeficiency syndrome and is caused by both the disease and the opportunistic infections that cause diarrhea, malabsorption and caloric deficit, resulting in loss of body fat, muscular protein breakdown and a decrease in lean body mass.[56] A poor nutritional state further contributes to increased susceptibility to infection in these patients.

It has been postulated that the wasting syndrome in AIDS is due to a lack of essential fatty acids, particularly gamma linoleic acid and/or isopentoic acid, brought about by deficient dietary intake, malabsorption and the presence of inhibitors of delta-6-desaturase enzyme activity in the gastrointestinal tract. The essential free fatty acid deficiency causes immunosuppression, increasing the susceptibility to viral infection.

According to the Task Force on Nutritional Support in AIDS,[56] nutritional therapy is mandatory when the wasting syndrome starts. If intestinal absorption is conserved, enteral feeding is possible. Total parenteral nutrition is indicated in the presence of chronic diarrhea or weight loss that occurs despite normal oral intake. Total parenteral nutrition is also indicated during the early course of AIDS to prevent progressive weight loss, to reduce the frequency of secondary infection, to augment response to chemotherapy, to improve the quality of life and sense of well-being and, ultimately, to retard progressive immunologic deterioration. Randomized prospective data to refute or support the role of aggressive nutritional support are pending.

In addition to being a caloric resource, fat emulsions are thought to have other beneficial effects. For example, fluidization of human immunodeficiency virus (HIV) membranes through cholesterol extraction may decrease the infectivity of the virus.[57] Thus, long-term intravenous nutrition may be more than a treatment for malabsorption and depletion. It may have direct pharmacologic effects that enhance the immune system and inactivate HIV.

CRITICAL ILLNESS

A number of major metabolic alterations contribute to the muscle wasting that occurs with critical illness. Among these are glucose intolerance, increased fat mobilization and increased protein breakdown. The effects of these changes are compounded because critically ill patients are frequently unable to take in nutrients through the gastrointestinal tract. Nutrition depletion may be further worsened if overwhelming septic complications are present.

Total parenteral nutrition can prevent loss of body mass and maintain or restore an optimal nutrition status. It is difficult, however, to define the role of total parenteral nutrition in modifying morbidity and mortality, except in patients with closed head injuries. In this situation, the early use of total parenteral nutrition has been found to result in fewer complications and enhanced survival, as compared with that in control subjects receiving oral feeding.[58]

It has been shown that BCAA-enriched total parenteral nutrition decreases muscular protein breakdown, increases protein synthesis in the liver and improves nitrogen retention in surgically stressed and post-trauma patients.[54] Because glucose intolerance may preclude the administration of high doses of glucose, 30 to 50 percent of nonprotein energy should be provided by fat.[59]

NEONATAL AND PEDIATRIC PATIENTS

Infants and children are less tolerant to starvation than adults, so any nutritional insult may exert a severe negative influence on organ development, especially the brain. For this reason, independent of an underlying disease, total parenteral nutrition is usually started sooner in pediatric patients than in adults.

Most of the reports on total parenteral nutrition in pediatric patients deal with low-birth-weight infants, in whom an immature intestinal tract is unable to process full nutrition loads. The general conclusion of these studies is that the use of total parenteral nutrition as an adjunct to different enteral formulas has a positive effect on weight gain but does not alter morbidity or duration of survival in low-birth-weight infants.[60] Conversely, total parenteral nutrition is effective in reducing the mortality rate in a variety of disorders, including gastroschisis,[61] short-bowel syndrome[62] and necrotizing enterocolitis.[63] Other indications for the use of total parenteral nutrition in infants and children are similar to those encountered in adults.

HOME USE

The decision to initiate home use of total parenteral nutrition depends on the patient’s primary diagnosis and clinical condition, and a support system for maintaining care in the home.

On the basis of the OASIS report on parenteral and enteral nutrition,[64] an estimated 14,300 patients were receiving home nutritional support in 1986. Home therapy was used in patients with cancer, Crohn’s disease, short-bowel syndrome and other gastrointestinal tract motility disorders. Nutrition support in patients with non-malignant diseases tends to be for years; in patients with cancer, AIDS and neurologic disorders, the duration is usually less than one year. The survival rate of patients receiving home nutrition support for non-neoplastic diseases is estimated at 60 to 80 percent at three years, with an 85 to 100 percent rate of rehabilitation.

In the absence of controlled clinical trials carefully evaluating the cost-effectiveness of home nutrition support, the guidelines for its use should take into account not only the general indications outlined for in-hospital total parenteral nutrition but also the motivation of both the patient and family to assume the responsibility of learning how to safely administer this complex treatment modality.

Complications

Nutrition support teams have had a great impact on reducing the complications from total parenteral nutrition. In a study conducted before the development of these teams, mechanical, septic and metabolic complications averaged 33 percent, 21 percent and 36 percent, respectively. After institution of these teams, complication rates fell dramatically to 3.2 percent, 6.5 percent and 3.0 percent, respectively.[65]

The rate of mechanical complications is directly related to the skill and experience of the person inserting the catheter. Other factors contributing to complications include the site of catheter insertion and the catheter material. Of 39,180 central venous catheters, mechanical complications were most frequent with a subclavian central venous insertion,[66] as shown in Table 2. The death rate related to central venous catheter complications was 1.2 percent. The safest method of obtaining central venous access is through the internal jugular vein, although this is not the most widely used route.

TABLE 2

Complications Associated with Total Parenteral Nutrition

Complication Nature Frequency

Mechanical Catheter tip malposition 6

Arterial laceration 1.4

Pneumothorax, hydrothorax or 1.1

hemothorax

Subclavian or superior vena 0.3

cava thrombosis

Thrombophlebitis 0.1

Catheter embolism 0.1

Septic Catheter-related sepsis 7.4

Acute metabolic Hyperglycemia/hypoglycemia Avoidable

Blood electrolyte abnormalities

Fluid overload

Hyperlipidemia

Related to Metabolic bone disease Rare

prolonged use Alteration in bile composition

Deterioration of liver function

The frequency of catheter sepsis is 7.4 percent. Quantitative blood culture is the most effective method for determining in situ catheter-related sepsis. In one study of catheter sepsis,[67] catheter removal was followed by improvement in the patient’s condition when the catheter was incriminated by culture data. In no instance when the central venous catheter was deemed “innocent” did its removal lead to clinical improvement.

Since total parenteral nutrition can be regarded as a sophisticated form of fluid and electrolyte therapy, many of the metabolic complications that were reported resulted from errors of omission. Thus, complications due to an excess or deficit of electrolytes, vitamins or trace elements are potentially avoidable. The introduction of a safe and reliable fat source has obviated metabolic complications derived from glucose-based parenteral nutrition,[59] such as hyperglycemia, hypoglycemia, hyperosmolar syndromes, hypertriglyceridemia, hyperlipidemia, hyperinsulinemia, elevated epinephrine, elevated liver function tests, hypercarbia,[68] essential fatty acid deficiencies and venous thrombosis.

TABLE I

Guidelines for the Use of Total Parenteral Nutrition Short-bowel syndrome Essential to achieve long-term stability in the critical

postoperative period; ensures survival. May be used temporarily or throughout life, depending on

adaptation of remaining functional gut. Perioperative Preoperative: two to three days of total parenteral nutrition

before surgery does not improve surgical outcome. Some improvement is observed with five to seven days of use. A significant reduction in major postoperative complications

and mortality is achieved with seven to 10 days of use before

surgery. Postoperative: when the anticipated period of postoperative

functional starvation exceeds five days. Inflammatory bowel disease For patients with Crohn’s disease who have gut failure and in

pediatric patients with growth failure. Can induce remission in 60 to 70 percent of patients with acute

flare-ups of Crohn’s disease but does not influence outcome

in severe complications of Crohn’s disease or the severe flare-ups

of chronic ulcerative colitis. Is indicated as adjuvant therapy in patients with chronic

ulcerative colitis and malnutrition who cannot otherwise

meet their nutritional needs. Enteral feeding with a defined formula diet is beneficial and

preferred to total parenteral nutrition in patients with active

Crohn’s disease. Enterocutaneous fistula Can control and reduce fistula output in conjunction with

somatostatin (Reducin), while preventing or treating local

skin complications and systemic metabolic and septic

complications. Prevents malnutrition and corrects volume, electrolyte and

acid-base deficits with intravenous fluid and electrolytes

when oral intake is stopped. Pancreatitis Is not required if the anticipated period of administration is less

than five to seven days. Is effective as nutritional support in necrotizing pancreatitis

and beneficial if complications arise. Data indicate safety of lipid emulsions in patients with acute

pancreatitis who have increased cholesterol and triglyceride

levels. Cancer Is not routinely indicated in well-nourished or mildly

malnourished patients undergoing surgery, chemotherapy

or radiation therapy. Useful for severely malnourished patients or patients whose

severe gastrointestinal or other toxicities preclude adequate

enteral intake for seven days or longer. Should be given prior to or in conjunction with the institution

of cancer therapy. Seldom indicated in patients with advanced cancer who have

significant deterioration of performance status or in patients

unresponsive to antineoplastic therapy. Not indicated in terminal disease or when no further

antineoplastic therapy is available. Beneficial in malnourished patients with cancer who can be

expected to have a normal or near-normal period of greater

than six months. Bone marrow transplantation In patients undergoing bone marrow transplantation, enhances

survival, diminishes relapse and shortens hospital stay. Cardiac surgery Overnight administration before coronary artery bypass graft

surgery increases myocardial glycogen content and

decreases postoperative morbidity and mortality. Obstetrics For patients with hyperemesis gravidarum. Is useful in exacerbations of preexisting conditions, such as

inflammatory bowel disease and pancreatitis, and in cases of

traumatic maternal death with a viable fetus. Acute renal failure Assists patients in coping with the abnormal intermediate

metabolism of acute renal failure until satisfactory renal

function returns. Formulas enriched with essential amino acids are not

unequivocally accepted. Advanced chronic liver failure For nutritionally depleted patients who are unable to tolerate

enteral nutrition. Prevents the secondary effects of starvation on general

metabolism and the liver. BCAA-enriched solution can be used to achieve proper

amino acid intake and avoid complications of hepatic

encephalopathy in patients unable to tolerate 60 to 80 g

of amino acids in regular solutions because of grade 3 or

4 hepatic encephalopathy. Acquired immunodeficiency syndrome For patients with malnutrition caused by anorexia or impaired

intestinal absorption, if enteral nutrition is unsuccessful. Routine use is discouraged because of a lack of data

documenting a positive influence on morbidity and

mortality. Critical care For well-nourished critically ill patients with a survivable

injury who are unable to eat or attain adequate enteral intake

within five to seven days or in previously malnourished

patients for whom it would be beneficial before the

hypermetabolic phase of recovery in a critical illness. Is of little benefit in critically ill patients whose hypermetabolic

phase is less than four or five days or when adequate enteral

nutrition is anticipated during this time. Is of no benefit in patients with a nonsurvivable injury, where

its use might prolong life unnecessarily. Pediatrics To prevent a severe negative influence on growth and organ

development in the absence of sufficient enteral nutrition. Use after three days if adjunctive enteral feedings are not well

tolerated and minimal caloric requirements cannot be met. Home use Improves quality of life and decreases cost of treatment.

REFERENCES

[1.] Campos AC, Paluzzi M, Meguid MM. The clinical use of total nutritional admixtures. Nutrition 1990;6:347-56. [2.] Evaluating total parenteral nutrition: core statement of the Technology Assessment and Practice Guidelines Forum. Nutrition 1990; 6:475-91. [3.] Campos AC, Meguid MM. A critical appraisal of the usefulness of perioperative nutritional support. Am J Clin Nutr 1992;55:117-30. [4.] Chandra RK. Immune responses in undernutrition and overnutrition: basic considerations and applied significance. Nutrition 1989; 5:297-302. [5.] Meguid MM, Campos AC, Meguid V, Debonis D, Terz JJ. IONIP, a criterion of surgical outcome and patient selection for perioperative nutritional support. Br J Clin Pract 1988; 63:8-14. [6.] Meguid MM, Campos AC, Hammond WG. Nutrition support in surgical practice. Part I. Am J Surg 1990; 159:345-58. [7.] Meguid MM, Campos AC, Hammond WG. Nutritional support in surgical practice. Part II. Am J Surg 1990; 159:427-43. [8.] Messing B, Colombel JF, Heresbach D, Chazouilleres O, Galian A. Chronic cholestasis and macronutrient excess in patients treated with prolonged parenteral nutrition. Nutrition 1992;8:30-6. [9.] Mughal MM, Meguid MM. The effect of nutritional status on morbidity after elective surgery for benign gastrointestinal disease. JPEN 1987;11:140-3. [10.] Holter AR, Fischer JE. The effects of perioperative hyperalimentation on complications in patients with carcinoma and weight loss. J Surg Res 1977;23:31-4. [11.] Muller JM, Brenner U, Dienst C, Pichlmaier H. Preoperative parenteral feeding in patients with gastrointestinal carcinoma. Lancet 1982; 1(8263):68-71. [12.] Moghissi K, Hornshaw J, Teasdale PR, Dawes EA. Parenteral nutrition in carcinoma of the oesophagus treated by surgery: nitrogen balance and clinical studies. Br J Surg 1977;64: 125-8. [13.] Heatley RV, Williams RH, Lewis MH. Preoperative intravenous feeding–a controlled trial. Postgrad Med J 1979; 55:541-5. [14.] Detsky AS, Jeejeebhoy KN. Cost-effectiveness of preoperative parenteral nutrition in patients undergoing major gastrointestinal surgery. JPEN 1984;8:632-7. [15.] Bellantone R, Doglietto GB, Bossola M, et al. Preoperative parenteral nutrition in the high risk surgical patient. JPEN 1988;12:195-7. [16.] Perioperative total parenteral nutrition in surgical patients. Veterans Affairs Total Parenteral Nutrition Cooperative Study Group. N Eng) J Med 1991;325:525-32. [17.] Collins JP, Oxby CB, Hill GL. Intravenous aminoacids and intravenous hyperalimentation as protein-sparing therapy after major surgery. A controlled clinical trial. Lancet 1978;1(8068):788-91. [18.] Preshaw RM, Attisha RP, Hollingsworth WJ. Randomized sequential trial of parenteral nutrition in healing of colonic anastomoses in man. Can J Surg 1979;22:437-9. [19.] Yamada N, Koyama H, Hioki K, Yamada T, Yamamoto M. Effect of postoperative total parenteral nutrition (TPN) as an adjunct to gastrectomy for advanced gastric carcinoma. Br J Surg 1983; 70:267-74. [20.] Reilly J, Ryan JA, Strole W, Fischer JE. Hyperalimentation in inflammatory bowel disease. Am J Surg 1976;131:192-200. [21.] Mullen JL, Hargrove WC, Dudrick SJ, Fitts WT Jr, Rosato EF. Ten years experience with intravenous hyperalimentation and inflammatory bowel disease. Ann Surg 1978;187: 523-9. [22.] Whittaker JS. Nutritional therapy of hospitalized patients with inflammatory bowel disease. Dig Dis Sci 1987; 32(12 Suppl): 89S-94S. [23.] Dickinson RJ, Ashton MG, Axon AT, Smith RC, Yeung CK, Hill GL. Controlled trial of intravenous hyperalimentation and total bowel rest as an adjunct to the routine therapy of acute colitis. Gastroenterology 1980; 79:1199-204. [24.] McIntyre PB, Powell-Tuck J, Wood SR, et al. Controlled trial of bowel rest in the treatment of severe acute colitis. Gut 1986;27:481-5. [25.] Muller JM, Keller HW, Erasmi H, Pichlmaier H. Total parenteral nutrition as the sole therapy in Crohn’s disease–a prospective study. Br J Surg 1983; 70:40-3. [26.] Jones VA. Comparison of total parenteral nutrition and elemental diet in induction of remission of Crohn’s disease. Long-term maintenance of remission by personalized food exclusion diets. Dig Dis Sci 1987;32(12 Suppl): 100S-7S. [27.] Greenberg GR, Fleming CR, Jeejeebhoy KN, Rosenberg IH, Sales D, Tremaine WJ. Controlled trial of bowel rest and nutritional support in the management of Crohn’s disease. Gut 1988;29:1309-15. [28.] Edmunds LH Jr, Williams GM, Welch CE. External fistulas arising from the gastrointestinal tract. Ann Surg 1960; 152:445-71. [29.] di Costanzo J, Cano N, Martin J, et al. Treatment of external gastrointestinal fistulas by a combination of total parenteral nutrition and somatostatin. JPEN 1987;11:465-70. [30.] Sax HC, Warner BW, Talamini MA, et al. Early total parenteral nutrition in acute pancreatitis: lack of beneficial effects. Am J Surg 1987;153:117-24. [31.] Grant JP, James S, Grabowski V, Trexler KM. Total parenteral nutrition in pancreatic disease. Ann Surg 1984;200:627-31. [32.] Blackburn GL, Williams LF, Bistrian BR, et al. New approaches to the management of severe acute pancreatitis. Am J Surg 1976; 131:114-24. [33.] Kirby DF, Craig RM. The value of intensive nutritional support in pancreatitis. JPEN 1985; 9:353-7. [34.] Torosian MH, Mullen JL, Miller EE, Zinsser KR, Stein TP, Buzby GP. Enhanced tumor response to cycle-specific chemotherapy by parenteral amino acid administration. JPEN 1983;7:337-45. [35.] Cheraskin E, Ringsdorf WM Jr, Hutchins K, Setyaamadja AT, Wideman GL. The effect of diet upon radiation response in cervical carcinoma of the uterus. A preliminary report. Acta Cytol 1968; 12:433-8. [36.] Ford JH Jr, Dudan RC, Bennett JS, Averette HE. Parenteral hyperalimentation in gynecologic oncology patients. Gynecol Oncol 1972; 1:70-5. [37.] Rossi-Fanelli F, Franchi F, Mulier M, et al. Effect of energy substrate manipulation on tumor cell proliferation in parenterally fed cancer patients. Clin Nutr 1991; 10:228-32. [38.] Donaldson SS, Lenon RA. Alterations of nutritional status: impact of chemotherapy and radiation therapy. Cancer 1979;43(5 Suppl): 2036-52. [39.] McDonald GB, Shulman HM, Sullivan KM, Spencer GD. Intestinal and hepatic complications of human bone marrow transplantation. Part I. Gastroenterology 1986;90:460-77. [40.] Aker SN, Cheney CL, Sanders JE, Lenssen PL, Hickman RO, Thomas ED. Nutritional support in marrow graft recipients with single versus double lumen right atrial catheters. Exp Hematol 1982; 10: 732-7. [41.] Weisdorf SA, Lysne J, Wind D, et al. Positive effect of prophylactic total parenteral nutrition on long-term outcome of bone marrow transplantation. Transplantation 1987;43 833-8. [42.] Iyengar SR, Charrette EJ, Iyengar CK, Wasan S. Myocardial glycogen in prevention of peri operative ischemic injury of the heart: a preliminary report. Can J Surg 1976; 19:246-51. [43.] Lolley DM, Ray JF 3d, Myers WO, Sheldo G, Sautter RD. Reduction of intraoperative myocardial infarction by means of exogenous anaerobic substrate enhancement: prospective randomized study. Ann Thorac Surg 1978;26:515-24. [44.] Rayburn W, Wolk R, Mercer N, Roberts J. Parenteral nutrition in obstetrics and gynecology. Obstet Gynecol Surv 1986; 41:200-14. [45.] Rainford DJ. Nutritional management of acute renal failure. Acta Chir Scand Suppl 1981; 507:327-9. [46.] Asbach HW, Stoeckel H, Schuler HW, et al. The treatment of hypercatabolic acute renal failure by adequate nutrition and haemodialysis. Acta Anaesthesiol Scand 1974;18:255-63. [47.] Abel RM, Beck CH Jr, Abbott WM, Ryan JA Jr, Barnett GO, Fischer JE. Improved survival from acute renal failure after treatment wit intravenous essential L-amino acids and glucose. Results of a prospective double-blind study. N Engl J Med 1973;288:695-9. [48.] Feinstein El, Blumenkrantz MJ, Healy M, et al. Clinical and metabolic responses to parenteral nutrition in acute renal failure. A controlled double-blind study. Medicine 1981; 60:124-37. [49.] Muscaritoli M, Cangiano C, Cascino A, et al. Exogenous lipid clearance in compensated liver cirrhosis. JPEN 1986;10:599-603. [50.] Ceci F, Muscaritoli M, Cangiano C, Familiari M, Rossi-Fanelli F. Effect of exogenous triglyceride infusion on the plasma amino acid profile in liver cirrhosis. Clin Nutr 1988;7: 151-6. [51.] Fischer JE, Funovics JM, Aguirre A, et al. The role of plasma amino acids in hepatic encephalopathy. Surgery 1975;78:276-90. [52.] Fischer JE, Rosen HM, Ebeid AM, James JH, Keane JM, Soeters PB. The effect of normalization of plasma amino acids on hepatic encephalopathy in man. Surgery 1976;80:77 91. [53.] Rossi-Fanelli F, Riggio O, Cangiano C, et al Branched-chain amino acids vs. lactulose in the treatment of hepatic coma: a controlled study. Dig Dis Sci 1982;27:929-35. [54.] Cerra FB, Cheung NK, Fischer JE, et al. Dis ease-specific amino acid infusion (F080) in hepatic encephalopathy: a prospective randomized, double-blind, controlled trial. JPEN 1985; 9:288-95. [55.] Naylor CD, O’Rourke K, Detsky AS, Baker JP. Parenteral nutrition with branched-chain amino acids in hepatic encephalopathy. A meta-analysis. Gastroenterology 1989;97: 1033-42. [56.] Task Force on Nutritional Support in AIDS. Guidelines for nutritional support in AIDS. Nutrition 1989;5:39-46. [57.] Begin ME, Das UN. A deficiency in dietary gamma-linoleic and/or eicosapantaenoic acids may determine individual susceptibility to AIDS. Med Hypoth 1986;20:1-8. [58.] Young B, Ott L, Twyman D, et al. The effect of nutritional support on outcome from severe head injury. J Neurosurg 1987;67:668-76. [59.] Meguid MM, Akahoshi M, Jeffers S, Hayashi RJ, Hammond WG. Amelioration of metabolic complications of conventional total parenteral nutrition. A prospective randomized study. Arch Surg 1984;119:1294-8. [60.] Gunn T, Reaman G, Outerbridge EW, Colle E. Peripheral total parenteral nutrition for premature infants with the respiratory distress syndrome: a controlled study. J Pediatr 1978; 92:608-13. [61.] Wagner CW, Parrish RA. Gastroschisis. Am Surg 1981;47:174-7. [62.] Wilmore DW. Factors correlating with a successful outcome following extensive intestinal resection in newborn infants. J Pediatr 1972; 80:88-95. [63.] Orenstein SR. Enteral versus parenteral therapy for intractable diarrhea of infancy. A prospective, randomized trial. J Pediatr 1986; 109:277-86. [64.] OASIS. Home nutritional support patient registry: annual report 1986 data. Silver Spring, Md.: The Oley Foundation and American Society for Parenteral and Enteral Nutrition, 1988. [65.] Nehme AE. Nutritional support of the hospitalized patient. The team concept. JAMA 1980;243:1906-8. [66.] Burri C, Ahnefeld FW. The caval catheter. New York: Springer-Verlag, 1977. [67.] Mosca R, Curtas S, Forbes B, Meguid MM. The benefits of Isolator cultures in the management of suspected catheter sepsis. Surgery 1987;102:718-23. [68.] Askanazi J, Rosenbaum SH, Hyman AI, et al. Effects of total parenteral nutrition on gas exchange and breathing patterns [Abstract]. Crit Care Med 1979;7:125.

MICHAEL M. MEGUID, M. D., PH. D. is professor of surgery and director of the Surgical Metabolism and Nutrition Laboratory at the State University of New York Health Science Center, Syracuse, N.Y. Dr. Meguid graduated from University College Hospital Medical School at the University of London, England, and completed a residency in surgery and a fellowship in surgical metabolism at Peter Bent Brigham University Hospital/Harvard Medical School, Boston.

MAURIZIO MUSCARITOLI, M.D. is assistant professor at State University of New York Health Science Center. He graduated f rom the University of Rome La Sapienza School of Medicine, where he also completed a residency in internal medicine and nephrology. Dr. Muscaritoli completed a fellowship in nutrition and metabolism at the Italian Ministry for Public Instruction in Rome.

COPYRIGHT 1993 American Academy of Family Physicians

COPYRIGHT 2004 Gale Group