Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Total parenteral nutrition Robert E. Hodges To cite this article: Robert E. Hodges (1979) Total parenteral nutrition, Postgraduate Medicine, 65:3, 171-180, DOI: 10.1080/00325481.1979.11715091 To link to this article: http://dx.doi.org/10.1080/00325481.1979.11715091
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Total parenteral nutrition An important therapeutic advance
RobertE. Hodges, MD
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Consider What are the indications for parenteralfeeding? Contraindications? What tests are usefulfor monitoring patients receiving TPN? What is the most common complication ofTPNtherapy?
VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
Total parenteral nutrition is an effective method of maintaining good nutritional status in a wide variety of conditions. The hazards involved in its administration can he minimized by a team approach and use of a strict protocol. Until recent years, progressive wasting was the fate of many persons who sustained a serious injury or underwent a major surgical procedure. The pioneering work of Cuthbertson1 in the 1930s showed not only the·heavy loss of nitrogen that accompanies a major fracture but also the ability of good nutritional care to reduce the magnitude of such loss. The remedy seemed to be administration of extra protein. For half a century, however, amino acids in the form of protein hydrolysates bad been given to patients in a catabolic state but bad not restored weight or depleted plasma proteins and bad not corrected anemia. The obvious need was for sources of energy adequate to protect amino acids from deamination and to support protein anabolism.2 Many imaginative schemes were devised. Ethyl alcohol, which provides 7 kcal/ gm, was added to infusa tes, but it caused inebriation and liver damage. Fat emulsions, studied during the 1950s, showed promise, but when toxicity became evident in sorne patients,3 use ofthese substances was curtailed in the United States. The problem was frustrating, and practical solutions were not obvious. Negative factors were the limited amounts of fluid that could be safely infused into pe-
ripheral veins and the irritating effects of concentrated glucose solutions on the venous endothelium. In the 1960s Dudrick and his group4,s showed that hypertonie solutions of dextrose and amino acids could be infused into the superior vena cava without producing fluid overload or venous thrombosis. Their studies, first in puppies and theo in an infant with a congenital defect of the digestive tract, clearly demonstrated that parenteral feeding as the sole source of nutrients could sustain growth and development in the young and restore lost weight in adults. This work bas led to a wide variety of applications of total parenteral nutrition (TPN) and to a better understanding of the nutritional needs of both children and adults. 6-s Another fortunate outcome bas been renewed interest in nutrition as an integral part of medicine and surgery. New applications of TPN have been reported almost every month as investigators have discovered that optimal nutrition benefits every patient.9,IO Indications for parenteral feeding New forms of therapy are likely to be accepted with enthusiasm; theo, as experience is acquired, the negative aspects become evident. Eventually, advantages and disadvancontinued 171
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Total parenteral nutrition is especially effective in newborns who fa il to thrive, in infants with diarrhea, and in adults with intestinal fistula, bowel obstruction, or pancreatitis.
Table 1. Clrcumstances in which total parenteral nutrition is contraindicated or has low benefitlrisk ratio Contralndicated when: Patient is able to eat orto receive adequate nutrition via gavage Patient has been in good nutritional health and can resume eating in a few da ys Patient has no chance for recovery or reasonable palliation Benefltlrlsk ratio is low when: Systemic sepsis is present, such as that occurring with massive burns or widespread neoplasia Hepatic coma is impending Patient is psychotic or uncooperative Fluid overload is present, such as syndrome of inappropriate secretion of antidiuretic hormone or congestive cardiac failure
Table 2. Vltamins and minerais to be added to total parenteral nutrition solutions* Vltamins Ascorbic acid Dexpanthenol Ergocalciferol Niacinamide Pyridoxine Riboflavin Thiamine Vitamin A VitaminE
Amountldayt 300mg 16.5 mg 660 usP units 60mg 9.9mg 6.6mg 33mg 6,600 usP units 3.31U
Minerais Calcium Chio ride Magnesium Phosphorus Potassium Sodium
Amountlday 20 mEq 150 mEq 16mEq 40mEq 85 mEq 120 mEq
'Note that vitam in K, folie ac id, and vitam in B 12 are not included, nor are essential fatty ac ids, and th at the amou nt of vitam in E is low. The pharmacist should add appropriate amounts of vitam in B 12 and folie acid to the solution and each patient should receive an intramuscular injection of a vitam in K preparation, such as AquaMephyton (10 mg), once a week. Administration of fat emulsion (lntralipid) will provide both essential fatty acids and additional vitaminE. Trace minerais, including copper and zinc, have been given by sorne clinicians but no commercial preparation is available. tAmounts are not optimal but representa compromise necessitated by the composition of available preparations of vitamins for intravenous administration.
tages can be compared and the true benefit/risk ratio determined. Considerable enthusiasm greeted earl y reports of successful parenteral feeding, 11 ·12 and physicians used TPN in a wide variety of disorders. 13-18 However, the meticulous care and strict protocol advocated by Dudrick and others were sornetimes ignored. The result was a high incidence of complications, especially infections. 172
Now a decade has passed and physicians have a much clearer idea of what TPN can and cannot do. The general principles of therapy are firmly established and most complications can be avoided. Accumulated experience and published reports19-29 have provided guidelines for determining the benefit likely in a given patient. Dudrick in his many publications has emphasized that the patient who
cannot eat, who should not eat, who will not eat, or who cannot eat enough may be a candidate for TPN. Others 17·19 have classified indications for TPN in various ways, eg: 1. Supportive nutritional therapy for surgical patients (preoperatively or postoperatively) 2. Supportive nutritional therapy for nonsurgical conditions, such as coma, neoplasia, transient obstruction (pylorospasm), anorexia nervosa 3. Primary therapy for conditions such as bowel fistula, pancreatitis, acute renal failure, impending hepatic coma, inflammatory bowel disease, irradiation enterocolitis TPN reportedly is very effective in newborns who fail to thrive, including sorne premature infants, and it is lifesaving in infants with gastroschisis who must undergo extensive surgical procedures. Jo TPN also has been highly effective in the management of infantile diarrhea. ln adults the best results have been obtained in patients with intestinal fistula; bowel obstruction or ileus; or diseases characterized by hypermotility, including malabsorption syndromes, short-bowel syndrome, and inflammatory bowel disease.JI-34 TPN often is helpful in patients with pancreatitis. Newer applications of TPN inelude therapy for burn patients and supportive treatment of patients receiving combination chemotherapy for malignancy. In acute and chronic renal failure and in hepatic failure TPN can be helpful but speVOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
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Infusion of TPN solution must be initiated with caution. lnitially, 40 gm of protein and 400 gm of glucose in 3 litera of water can be given at the rate of 1 liter/12 hr.lfthis is weil tolerated the concentration can be increased gradually to 60 to 1 00 gm of protein and 600 to 1 ,000 gm of glucose.
cial formulations and procedures are required. The decision to use TPN must be made by the physician in charge. In many instances, the physician may choose between parenteral and enterai feeding; sometimes a combination is indicated. Circumstances in which TPN is contraindicated or in which the benefitjrisk ratio is low are given in table 1. Method of use
The nutrient solution-Commercially available amino acid solutions consist of protein hydrolysates or mixtures of free (L) amino acids. Both have been shown to support protein anabolism in experimental animais and in human volunteers, but in the department of internai medicine at the University of California School of Medicine, Davis, we prefer to use free amino acids, especially in severe catabolism. In healthy subjects amino acids given alone !essen urinary Joss of nitrogen, but in catabolic patients an abundant supply of energy is needed to prevent deamination and foster protein synthesis. Investigators have advocated energy (kilocalorie)/ nitrogen ratios of from 100: 1 to 400:1 or even higher. We have adopted a middle-of-the-road figure of200:1. Nonprotein energy sources are glucose and fat. Although glucose ordinarily would provide about 4 kcal/ gm, pharmaceutical solutions are made with hydrated glucose,
which is 15% water. Therefore, the figure for glucose in solution should be 3.4 kcal/ gm. Th us, 200 kcal glucose: 1 gm nitrogen can be translated into 200/3.4 kcal glucose: 1 gm nitrogen =59 gm glucose:6.25 gm protein (proteinjnitrogen ratio= 6.25: 1). As a practical measure we use ten times as much glucose as protein (62.5 gm), which gives an energy /nitrogen ratio of 212. Appropriate amounts of vitamins35 and minerais (table 2) and water to make 3 liters of solution are added. The pharmacist, wearing sterile cap, mask, gown, and gloves, makes up the physician's prescription for TPN solution under strict aseptic conditions, with use of a Laminar air-flow hood. The TPN bottle should be regarded as a sealed unit and nothing should be added to it or piggybacked through it. Since TPN solutions are hypertonie, infusion must be started cautiously. For most patients we recommend that the initial solution contain 40 gm of protein and 400 gm of glucose in 3 liters of water, with only 2liters being given the first day (!liter/ 12 hr). If this amount is weil tolerated, the flow can be increased to 1 liter every eight hours. After two or three days if there is little or no glycosuria or hyperglycemia, the concentration can be increased to 60 gm of protein and 600 gm of glucose. Subsequently, if the patient's condition is satisfactory, 80 gm of protein and 800 gm of glucose and eventually lOO gm of protein
Robert E. Hodges Dr Hodges is professor, department of internai medicine, and chief, section of nutrition, University ofCalifornia School of Medicine, Davis.
and 1,000 gm of glucose can be given, if necessary, to achieve weight gain. Fat emulsion can be given in a peripheral vein to provide essential fatty acids and additional energy.3 Placement of catheter-The catheter should be flexible, radiopaque, and nonwettable to reduce formation of fi brin sheath. lt may be made of silicone, polytetrafluoroethylene, or polyvinyl.I2,36 Catheter insertion should be done as a sterile surgical procedure by or under the supervision of a skilled opera tor. Both operator and assistant should wear masks and the opera tor should also wear sterile gloves. The procedure is done at the bedside with curtains drawn for isolation. The preferred site of catheter insertion in adults is the subclavian
continued VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
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Catheter insertion tor TPN is done as a sterile, surgical procedure. A local anesthetic is used, and the patient must pertorm the Valsalva maneuver during the procedure.
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Table 3. Oaily checklist for members of total parenteral nutrition (TPN) therapy team Examine label on TPN bottle to confirm thal it con tains correct formulation Check TPN flow rate Observe patient's appearance, color, mood, and orientation Check record of vital signs on bedside chart Check record of fluid intake and output and body weight Check results of fractional urine tests for glucose and acetone Check results of biochemical blood tests, especially determinations of glucose, inorganic phosphorus, and electrolyte levels Examine dressing covering site of infusion Read progress notes to maintain familiarity with patient's course, results of studies. and proposed plan Make appropriate notes in chart to keep nursing and medical staff informed about nutritional progress Table 4. Substances to be monitored in plasma or serum of patients receiving total parenteral nutrition SMA 6/60 test BUN Carbon dioxide Chio ride Glucose Potassium ,Sodium
SMA 12/60 test Album in Alkaline phosphatase Bilirubin Calcium Cholesterol Creatine phosphokinase
vein. The patient is placed in the Trendelenburg position with a rolled sheet between the scapulae to allow the shoulders to fall backward. The proposed puncture site is at the mid point of and about 1 to 2 cm below the clavicle. This area of skin is defatted with acetone and scrubbed for five minutes with an iodine solution, such as povidoneiodine (Betadine). During these preliminaries the operator reassures the patient, ex plains the procedure, and gives instruction in how to perform the Valsalva maneuver. The selected puncture site is anesthetized. The opera tor then places one finger in the suprasternal notch, punctures the skin with a needle on a syringe, and directs the needle taward the no teh, turning the bevel to174
Creatinine Lactic dehydrogenase Phosphorus SGOT Total protein Urie ac id
ward the patient's heart. When the needle bas been advanced slightly the patient is asked to perform the Valsalva maneuver; the subclavian vein is then punctured. As saon as blood flows into the syringe the operator grasps the needie with a hemostat, removes the syringe, and inserts the catheter, carefully threading it into the superior vena cava. Once the catheter is inserted to its hub, bath needle and catheter are slowly withdrawn until the needle can be removed. An infusion of isotonie saline or glucose solution is begun, the catheter is sutured to the skin, the area is carefully cleaned with povidone-iodine solution and alcohol, and a small a mount of povidone-iodine ointment is placed around the puncture
site. The area is covered with a sterile gauze sponge and the surrounding skin is sprayed with tincture of benzain and allowed to dry. A rectangle of semipermeable dressing, such as Elastoplast, is placed over the site. Only the edges are taped, th us permitting perspiration to evapora te through the central area. Infusion of isotonie solution is continued until an x-ray film confirms that the tip of the catheter is 1 to 2 cm above the right auricle. The hypertonie TPN solution is then connected to an in-line filter which, in turn, is connected to the catheter, and the junction is carefully taped.J7 The TPN solution will flow by gravity through a 0.45 J.L filter; if a constant flow rate is essential, a pump must be used.3 8 Monitoring The most effective way to monitor TPN therapy is to establish a team consisting of a special nurse, a pharmacist, and a physician. At !east one member of the team should visit the patient daily. The points to be checked are shawn in table 3. The team nurse supervises a change of dressing three times weekly. The same strict asepsis must be used as for catheter insertion.3 9
Laboratory monitoring-Urine should be collected four times daily at about six-hour intervals and each fraction tested for glucose and acetone. Results can be recorded conveniently on the same form as that used for diabetic patients. In most patients on! y small amounts of gluVOL 65/NO 3/MARCH 1979/POSTGRAOUATE MEDICINE
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After catheter insertion, an isotonie solution should be infused until an x-ray film verifies catheter position. Infusion of TPN solution then can be started.
cose will be found in the urine and then only for one to three da ys. Transient glycosuria may occur on initiation of TPN or when the dosage is increased. The blood glucose leve! is used to identify patients who have an abnormal renal threshold for glucose. Ordinarily, such patients do not need exogenous insulin, but if glycosuria persists (3+ to 4+) and the glucose leve! is in excess of 300 mg/ dl, insulin probably will be needed. We prefer to give Regular insulin in fixed rather than "sliding scale" doses because the method used to determine the latter is imprecise and therapy is often ineffective. We do not add insulin to the infusion fluid because the subcutaneous route is more dependable. Biachemica/ tests-The SMA 6/60and SMA 12/60tests(orequivalent tests) are very useful for monitoring patients receiving TPN (table 4). Aberrations in electrolyte levels may occur in patients who Jose large quantities of fluid as a result of gastric suction, diarrhea, or drainage from a fistula. We advise against late addition of electrolytes to the TPN solution and prefer to give the necessary supplements through a peripheral vein. Knowledge of blood glucose leve! is most important early in therapy, and th us the leve! should be checked daily for severa! days until it is stable, and then twice weekly. The S MA 12/60 test gives vital information and should be performed twice VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
a week initially, then once weekly. The BUN 1creatinine ratio is normany in the range of 10 to 20. A value below 10 may mean that insufficient protein is being given. A value above 20 may reflect either excessive protein intake or bleeding into the upper digestive tract. A CBC should be performed once each week. In anemie patients, total iron-binding capacity and levels of
serum iron, folate, and vitamin B12 should also be measured. Since TPN solutions do not contain appreciable amounts of iron, it may be necessary to give iron dextran injection (lmferon) either intramuscularly or intravenously. Few emaciated patients have sufficient muscle tissue to permit use of the intramuscular route. The initial intravenous dose should be only 25 mg, given slowly. continued
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During TPN therapy, urine must be monitored for glucose and acetone and blood for changes in electrolyte levels. A CBC should be done once a week. lntravenous fat emulsion should be given in a peripheral vein to patients who must receive TPN continuously for several weeks.
Figure 1. Oxidative metabolism of glucose.
This can be repeated on subsequent days untillOO mg has been given. Under no circumstances should iron be added to the TPN solution, because of incompatibility with other components. Since TPN solutions also lack vitamin K, prothrombin and partial thromboplastin times should be measured at regular intervals. If these tests indicate a need for vi tamin K, 10 mg of an injectable preparation, eg, AquaMephyton, can be given either intramuscularly or intravenously. Essential fatty acid deficiency develops in patients who receive TPN continuously for severa! weeks.40 It can be prevented by giving intrave178
nous fat emulsion (Intralipid) in a peripheral vein.at a rate of lOO ml/hr for a dosage of 500 ml/ day. This supplies an additional 550 kcal as weil. Deficiency of trace minerais, especially of zinc and copper,4t probably develops in most patients who receive TPN for periods longer than one month. At present there is no approved IV preparation for trace minerais, but several clinics have prepared supplements that apparently meet this need. Complications
Mechanical-The most common mechanical complication of TPN is pneumothorax, but any intratho-
racic structure within reach of the needle can be damaged. The catheter may injure the right auricle or the pericardium. Thrombosis of a venous structure is always a risk, albeit small. Accidentai cutting of the catheter by the sharp needle can resuit in catheter embolization. Metabo/ic-Hyperglycemia may result from too rapid infusion of TPN solution or from administration of a too-large dose of glucose to a starved patient who has not had time to adapt.42.43 Severe hyperglycemia may result in hyperosmolar coma. If TPN is stopped abruptly, hypoglycemia may ensue as a result of endogenous secretion of insulin. This usually occurs after sudden slowing of an infusion that bas been running at a rapid rate, and it emphasizes the need for a constant flow rate. Sorne degree of hypophosphatemia occurs whenever a large amount of carbohydrate is being metabolized. Normally the two molecules of phosphate that phosphorylate each molecule of glucose are recycled by the liver and homeostasis is maintained (figure 1),44,45 With continuous infusion of glucose, the demand for phosphate persists but the sustained insulin response prevents the normal recycling of phosphate. The result is hypophosphatemia accompanied by a falling level of 2,3-diphosphoglycerate in the RBCs, causing a shift to the left in the oxygen dissociation curve of hemoglobin and resulting in tissue hypoxia. Other effects of hypophosVOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
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Pneumothorax is the most common mechan· ical complication ofTPN.
phatemia include impairment of coagulation and phagocytosis and increased rigidity of RBC walls. Hypophosphatemia occurs chiefly in patients who have been starved before initiation of TPN. If aluminum hydroxide gel has been given orally, phosphate levels may have become depleted. Measure-· ment of the serum phosphorus leve! usually is diagnostic. Treatment must be prompt: The hypertonie infusion should be replaced by a solution of 5% dextrose and 0.9% saline to which 20 mEq of phosphate per liter has been added. This solution is given at a rate of 1 liter 112 hr; response should occur within 12 to 24 hours. As soon as the serum phosphorus leve! retums to normal, TPN can be resumed, first at a reduced rate and then at the normal rate. Infection-By far the most cornmon complication of TPN therapy is infection of the IV catheter.46-49 This results from two factors: ( 1) The indwelling catheter is a foreign body that soon becomes coated with a fibrin sheath, and (2) the TPN solution is an excellent culture medium that supports growth of bacteria and fungi. The incidence of primary infection can be reduced to less than 3% if a strict protocol is followed; incidence may rise to grea ter than 50% if no protocol is used. Fever in a patient receiving TPN presents a dilemma. The risk of permitting an infected line to remain in place is considerable, but removal of the line is undesirable. We have used the following protocol when VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
the temperature exceeds 100 F (38.4 C). 1. TPN solution, IV tubing, and filter are replaced, but the catheter is left in place and TPN is continued. 2. Three blood cultures are obtained at the peak of the febrile spikes during the next 24 hours. 3. Other sources of infection are sought: nose, throat, ears, sin uses, lungs, abdomen, urinary tract. 4. If fever continues and the cause is still obscure after 24 hours, the TPN catheter is assumed to be infected. Blood for culture is taken through the catheter, the catheter is removed, and the tip is cultured for bacteria and fungi. Usually TPN can be restarted immediately in the subclavian vein on the opposite side. In patients who have frequent episodes of bacteremia, such as those with burns, disseminated neoplasms, or multiple intraabdominal abscesses, it may be necessary to replace the catheter twice a week. Termination of TPN The decision to stop TPN may be based on an adverse reaction or on correction of the factors that dictated the need for therap . It is advisable that the rate of flow of the infusion be reduced for 24 hours before removal of the catheter and that a peripheral infusion of 10% dextrose in water, !liter in 12 hours, be given subsequently (under the assumption that the patient has begun to eat and can take feedings at intervals in the event of hypoglycemie symptoms).
Conclusion Total parenteral nutrition (TPN) is a potent form of therapy. It is particularly useful in patients who must undergo surgery or those with conditions that preclude normal feeding. The procedure is not without risk, but better understanding of the basic principles involved, refinements in technique, and experience with its use in different situations have combined to improve the results of therapy over those fmt obtained. TPN represents an important therapeutic advance and emphasizes the need for an understanding of nutritional principles by physicians and for a team approach to the management of complicated conditions. Address reprint requests to Robert E. Hodges, MD, Department of Internai Medicine, Section of Nutrition, University of California School of Medicine, Davis, CA 95616. References 1. Cuthbertson DP: Further observations on the disturbance of metabolism caused by injury, with particular reference to the dietary requirements of fracture cases. Br J Surg 23:505, 1936 2. Munro H: Basic concepts in the use of amino acids and protein hydrolysates for parenteral nutrition. IV. Additive review. Drug Intell Clin Pharm 6:216, 1972 3. Meng HC: Use of fat emulsions in parenteral nutrition. Drug Intell Clin Pharm 6:321, 1972 4. Dudrick SJ, Wilmore DW, Vars HM, et al: Long-term parenteral nutrition with growth, development and positive nitrogen balance. Surgery64:134,1968 S. Dudrick SJ, Wilmore DW, Vars HM, et al: Can intravenous feeding as the sole means of nutrition support growth in the child and re-
continued 179
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store weight Joss in an adult? An affirmative answer. Ann Surg 169:974, 1969 6. Cahil GF Jr, Felig P, Marliss EB: Sorne physiologie princip les of parenteral nutrition. In Fox CL, Nahas GG (Editors): Body Fluid Replacement in the Surgical Patient. New York, Grune & Stratton Inc, 1970, p 286 7. Vinnars E, Fürst P, Hermansson IL, et al: Protein catabolism in the postoperative state and its treatment with amino acid solutions. Acta Chir Scand 136:95, 1970 8. Hinton P, Allison SP, Littlejohn S, et al: Insulin and glucose to reduce catabolic response to injury in burned patients. Lancet 1:767, 1971 9. Turner FP: Intravenous hyperalimentation. (Letter) JAMA 223:441, 1973 10. Intravenous feeding. (Editorial) Lance! 2:1179, 1973 11. Dudrick SJ, Rhoads JE: New horizons for intravenous feeding. JAMA 215:939, 1971 12. Dudrick SJ, Ruberg RL: Principles and practice of parenteral nutrition. Gastroenterology 61:901, 1971 13. Meng HC: Princip les of parenteral nutrition. Hosp Med, Jan 1971, p 102 14. Owings JW, Bomar WE Jr, Ramage RC: Parenteral hyperalimentation and its practi-. cal applications. Ann Surg 175:712, 1972 15. Hutson DG, Zeppa R: Sorne observations on the use of parenteral alimentation. South Med J 65:583, 1972 16. Parsa MH, Habif DV, Ferrer JM, et al: Intravenous hyperalimentation: Indications, technique and complications. Bull NY Acad Med 48:920, 1972 17. Heird WC, Winters RW: Total intravenous alimentation. Am J Dis Child 126:287, 1973 18. Heird WC, Winters RW: Total parenteral nutrition: The state of the art. J Pediatr 86:2, 1975 19. Abbott WM: Indications for parenteral nutrition. In Fischer JE (Editor): Total Parenteral Nutrition. Boston, Little Brown & Co, 1976, p 3 · 20. Rush BF Jr, Richardson JD, Griffin WO Jr: Positive nitrogen balance immediately after abdominal operations. Am J Surg 119:70, 1970 21. McNamara JJ, Molot MD, Wissman D, et al: Intravenous hyperalimentation: An important adjunct in the treatment of combat
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casualties. Am J Surg 122:70, 1971 22. Steiger E, Allen TR, Daly JM, et al: Beneficiai effects of immediate postoperative total parenteral nutrition. Surg Forum 22:89, 1971 23. Irving MH, Rushman GB: Parenteral nutrition for the surgical patient. Anaesthesia 26:450, 1971 24. Wilmore DW, Curreri PW, Spitzer KW, et al: Supranorrnal dietary intake in therrnally injured hypermetabolic patients. Surg Gynecol Obstet 132:881, 1971 25. Van Way CW 3d, Meng HC, Sandstead HH: An assessment of the role of parenteral alimentation in the management of surgical patients. Ann Surg 177:103, 1973 26. Hindmarsh JT, Clark RG: The effects of intravenous and intraduodenal feeding on nitrogen balance after surgery. Br J Surg 60:589, 1973 27. Dolanski EA, Stahlman MT, Meng HC: Parenteral alimentation of premature infants under 1,200 grams. South Med J 66:41, 1973 28. Lloyd-Still JD, Shwachman H, Filler RM: Protracted diarrhea of infancy treated by intravenous alimentation. 1. Clinical results of 16 infants. Am J Dis Child 125:358, 1973 29. Popp MB, Law EJ, MacMillian BG: Parenteral nutrition in the burned child: A study oftwenty-six patients. Ann Surg 179:219, 1974 30. Lloyd-Still JD, Shwachman H, Filler RM: Intravenous hyperalimentation in pediatries. AmJ Dig Dis 17:1043, 1972• 31. Scribner BH, Cole JJ, Christopher TG, et al: Long-term total parenteral nutrition: The concept of an artificial gut. JAMA 212:457, 1970 32. MacFadyen BV Jr, Dudrick SJ, Ruberg RL: Management of gastrointestinal fistulas with parenteral hyperalimentation. Surgery 74:100, 1973 33. Vogel CM, Corwin TR, Baue AE: Intravenous hyperalimentation in the treatment of inflammatory diseases of the bowel. Arch Surg 108:460, 1974 34. Reilly J, Ryan JA, Strole W, et al: Hyperalimentation in inflammatory bowel disease. AmJSurg 131:192,1976 35. Greene HL: Vitamins in total parenteral nutrition. Drug lntell Clin Pharm 6:355, 1972 36. Dudrick SJ, Wilmore DW: Long-terrn parenteral feeding. Hosp Prac 3:65, 1968
37. Wilmore DW, Dudrick SJ: An in-tine filter for intravenous solutions. Arch Surg 99:462, 1969 38. Monohan JJ, Webb JW: lntravenous infusion pumps: An added dimension toparenteral therapy. Am J Hosp Pharrn 29:54, 1972 39. Parsa MH, Thomton BH, Ferrer JM: Central venous alimentation. Am J Nurs 72:2042, 1972 40. Fleming CR, Smith LM, Hodges RE: Essential fatty acid deficiency in adults receiving total parenteral nutrition. Am J Clin Nutr 29:976, 1976 41. Fleming CR, Hodges RE, Hurley LS: A prospective study of serum copper and zinc Ievels in patients receiving total parenteral nutrition. Am J Clin Nutr 29:70, 1976 42. Danowski TS, Nabarro JD: Hyperosmolar and other types of nonketoacidotic coma in diabetes. Diabetes 14:162, 1965 43. Dudrick SJ, MacFadyen BV Jr, Van Buren CT, et al: Parenteral hyperalimentation: Metabolic problems and solutions. Ann Surg 176:259, 1972 44. Silvis SE, Paragas PD Jr: Fatal hyperalimentation syndrome: Animal studies. J Lab Clin Med 78:918, 1971 45. Silvis SE, Paragas PD Jr: Paresthesias, weakness, seizures, and hypophosphatemia in patients receiving hyperalimentation. Gastroenterology 62:513, 1972 46. Ashcraft KW, Leape LL: Candida sepsis complicating parenteral feeding. JAMA 212:454, 1970 47. Boeckman CR, Krill CE Jr: Bacterial and fungal infections complicating parenteral alimentation in infants and children. J Pediatr Surg5:117, 1970 48. Goldmann DA, Maki DG, Rhame FS, et al: Guidelines for infection control in intravenous therapy. Ann Intern Med 79:848, 1973 49. Maki DG, Goldmann DA, Rhame FS: Infection control in intravenous therapy. Ann Intern Med 79:867, 1973
VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Total parenteral nutrition Robert E. Hodges To cite this article: Robert E. Hodges (1979) Total parenteral nutrition, Postgraduate Medicine, 65:3, 171-180, DOI: 10.1080/00325481.1979.11715091 To link to this article: http://dx.doi.org/10.1080/00325481.1979.11715091
Published online: 07 Jul 2016.
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [Australian Catholic University]
Date: 12 August 2017, At: 00:09
Total parenteral nutrition An important therapeutic advance
RobertE. Hodges, MD
Downloaded by [Australian Catholic University] at 00:09 12 August 2017
Consider What are the indications for parenteralfeeding? Contraindications? What tests are usefulfor monitoring patients receiving TPN? What is the most common complication ofTPNtherapy?
VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
Total parenteral nutrition is an effective method of maintaining good nutritional status in a wide variety of conditions. The hazards involved in its administration can he minimized by a team approach and use of a strict protocol. Until recent years, progressive wasting was the fate of many persons who sustained a serious injury or underwent a major surgical procedure. The pioneering work of Cuthbertson1 in the 1930s showed not only the·heavy loss of nitrogen that accompanies a major fracture but also the ability of good nutritional care to reduce the magnitude of such loss. The remedy seemed to be administration of extra protein. For half a century, however, amino acids in the form of protein hydrolysates bad been given to patients in a catabolic state but bad not restored weight or depleted plasma proteins and bad not corrected anemia. The obvious need was for sources of energy adequate to protect amino acids from deamination and to support protein anabolism.2 Many imaginative schemes were devised. Ethyl alcohol, which provides 7 kcal/ gm, was added to infusa tes, but it caused inebriation and liver damage. Fat emulsions, studied during the 1950s, showed promise, but when toxicity became evident in sorne patients,3 use ofthese substances was curtailed in the United States. The problem was frustrating, and practical solutions were not obvious. Negative factors were the limited amounts of fluid that could be safely infused into pe-
ripheral veins and the irritating effects of concentrated glucose solutions on the venous endothelium. In the 1960s Dudrick and his group4,s showed that hypertonie solutions of dextrose and amino acids could be infused into the superior vena cava without producing fluid overload or venous thrombosis. Their studies, first in puppies and theo in an infant with a congenital defect of the digestive tract, clearly demonstrated that parenteral feeding as the sole source of nutrients could sustain growth and development in the young and restore lost weight in adults. This work bas led to a wide variety of applications of total parenteral nutrition (TPN) and to a better understanding of the nutritional needs of both children and adults. 6-s Another fortunate outcome bas been renewed interest in nutrition as an integral part of medicine and surgery. New applications of TPN have been reported almost every month as investigators have discovered that optimal nutrition benefits every patient.9,IO Indications for parenteral feeding New forms of therapy are likely to be accepted with enthusiasm; theo, as experience is acquired, the negative aspects become evident. Eventually, advantages and disadvancontinued 171
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Total parenteral nutrition is especially effective in newborns who fa il to thrive, in infants with diarrhea, and in adults with intestinal fistula, bowel obstruction, or pancreatitis.
Table 1. Clrcumstances in which total parenteral nutrition is contraindicated or has low benefitlrisk ratio Contralndicated when: Patient is able to eat orto receive adequate nutrition via gavage Patient has been in good nutritional health and can resume eating in a few da ys Patient has no chance for recovery or reasonable palliation Benefltlrlsk ratio is low when: Systemic sepsis is present, such as that occurring with massive burns or widespread neoplasia Hepatic coma is impending Patient is psychotic or uncooperative Fluid overload is present, such as syndrome of inappropriate secretion of antidiuretic hormone or congestive cardiac failure
Table 2. Vltamins and minerais to be added to total parenteral nutrition solutions* Vltamins Ascorbic acid Dexpanthenol Ergocalciferol Niacinamide Pyridoxine Riboflavin Thiamine Vitamin A VitaminE
Amountldayt 300mg 16.5 mg 660 usP units 60mg 9.9mg 6.6mg 33mg 6,600 usP units 3.31U
Minerais Calcium Chio ride Magnesium Phosphorus Potassium Sodium
Amountlday 20 mEq 150 mEq 16mEq 40mEq 85 mEq 120 mEq
'Note that vitam in K, folie ac id, and vitam in B 12 are not included, nor are essential fatty ac ids, and th at the amou nt of vitam in E is low. The pharmacist should add appropriate amounts of vitam in B 12 and folie acid to the solution and each patient should receive an intramuscular injection of a vitam in K preparation, such as AquaMephyton (10 mg), once a week. Administration of fat emulsion (lntralipid) will provide both essential fatty acids and additional vitaminE. Trace minerais, including copper and zinc, have been given by sorne clinicians but no commercial preparation is available. tAmounts are not optimal but representa compromise necessitated by the composition of available preparations of vitamins for intravenous administration.
tages can be compared and the true benefit/risk ratio determined. Considerable enthusiasm greeted earl y reports of successful parenteral feeding, 11 ·12 and physicians used TPN in a wide variety of disorders. 13-18 However, the meticulous care and strict protocol advocated by Dudrick and others were sornetimes ignored. The result was a high incidence of complications, especially infections. 172
Now a decade has passed and physicians have a much clearer idea of what TPN can and cannot do. The general principles of therapy are firmly established and most complications can be avoided. Accumulated experience and published reports19-29 have provided guidelines for determining the benefit likely in a given patient. Dudrick in his many publications has emphasized that the patient who
cannot eat, who should not eat, who will not eat, or who cannot eat enough may be a candidate for TPN. Others 17·19 have classified indications for TPN in various ways, eg: 1. Supportive nutritional therapy for surgical patients (preoperatively or postoperatively) 2. Supportive nutritional therapy for nonsurgical conditions, such as coma, neoplasia, transient obstruction (pylorospasm), anorexia nervosa 3. Primary therapy for conditions such as bowel fistula, pancreatitis, acute renal failure, impending hepatic coma, inflammatory bowel disease, irradiation enterocolitis TPN reportedly is very effective in newborns who fail to thrive, including sorne premature infants, and it is lifesaving in infants with gastroschisis who must undergo extensive surgical procedures. Jo TPN also has been highly effective in the management of infantile diarrhea. ln adults the best results have been obtained in patients with intestinal fistula; bowel obstruction or ileus; or diseases characterized by hypermotility, including malabsorption syndromes, short-bowel syndrome, and inflammatory bowel disease.JI-34 TPN often is helpful in patients with pancreatitis. Newer applications of TPN inelude therapy for burn patients and supportive treatment of patients receiving combination chemotherapy for malignancy. In acute and chronic renal failure and in hepatic failure TPN can be helpful but speVOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
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Infusion of TPN solution must be initiated with caution. lnitially, 40 gm of protein and 400 gm of glucose in 3 litera of water can be given at the rate of 1 liter/12 hr.lfthis is weil tolerated the concentration can be increased gradually to 60 to 1 00 gm of protein and 600 to 1 ,000 gm of glucose.
cial formulations and procedures are required. The decision to use TPN must be made by the physician in charge. In many instances, the physician may choose between parenteral and enterai feeding; sometimes a combination is indicated. Circumstances in which TPN is contraindicated or in which the benefitjrisk ratio is low are given in table 1. Method of use
The nutrient solution-Commercially available amino acid solutions consist of protein hydrolysates or mixtures of free (L) amino acids. Both have been shown to support protein anabolism in experimental animais and in human volunteers, but in the department of internai medicine at the University of California School of Medicine, Davis, we prefer to use free amino acids, especially in severe catabolism. In healthy subjects amino acids given alone !essen urinary Joss of nitrogen, but in catabolic patients an abundant supply of energy is needed to prevent deamination and foster protein synthesis. Investigators have advocated energy (kilocalorie)/ nitrogen ratios of from 100: 1 to 400:1 or even higher. We have adopted a middle-of-the-road figure of200:1. Nonprotein energy sources are glucose and fat. Although glucose ordinarily would provide about 4 kcal/ gm, pharmaceutical solutions are made with hydrated glucose,
which is 15% water. Therefore, the figure for glucose in solution should be 3.4 kcal/ gm. Th us, 200 kcal glucose: 1 gm nitrogen can be translated into 200/3.4 kcal glucose: 1 gm nitrogen =59 gm glucose:6.25 gm protein (proteinjnitrogen ratio= 6.25: 1). As a practical measure we use ten times as much glucose as protein (62.5 gm), which gives an energy /nitrogen ratio of 212. Appropriate amounts of vitamins35 and minerais (table 2) and water to make 3 liters of solution are added. The pharmacist, wearing sterile cap, mask, gown, and gloves, makes up the physician's prescription for TPN solution under strict aseptic conditions, with use of a Laminar air-flow hood. The TPN bottle should be regarded as a sealed unit and nothing should be added to it or piggybacked through it. Since TPN solutions are hypertonie, infusion must be started cautiously. For most patients we recommend that the initial solution contain 40 gm of protein and 400 gm of glucose in 3 liters of water, with only 2liters being given the first day (!liter/ 12 hr). If this amount is weil tolerated, the flow can be increased to 1 liter every eight hours. After two or three days if there is little or no glycosuria or hyperglycemia, the concentration can be increased to 60 gm of protein and 600 gm of glucose. Subsequently, if the patient's condition is satisfactory, 80 gm of protein and 800 gm of glucose and eventually lOO gm of protein
Robert E. Hodges Dr Hodges is professor, department of internai medicine, and chief, section of nutrition, University ofCalifornia School of Medicine, Davis.
and 1,000 gm of glucose can be given, if necessary, to achieve weight gain. Fat emulsion can be given in a peripheral vein to provide essential fatty acids and additional energy.3 Placement of catheter-The catheter should be flexible, radiopaque, and nonwettable to reduce formation of fi brin sheath. lt may be made of silicone, polytetrafluoroethylene, or polyvinyl.I2,36 Catheter insertion should be done as a sterile surgical procedure by or under the supervision of a skilled opera tor. Both operator and assistant should wear masks and the opera tor should also wear sterile gloves. The procedure is done at the bedside with curtains drawn for isolation. The preferred site of catheter insertion in adults is the subclavian
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Catheter insertion tor TPN is done as a sterile, surgical procedure. A local anesthetic is used, and the patient must pertorm the Valsalva maneuver during the procedure.
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Table 3. Oaily checklist for members of total parenteral nutrition (TPN) therapy team Examine label on TPN bottle to confirm thal it con tains correct formulation Check TPN flow rate Observe patient's appearance, color, mood, and orientation Check record of vital signs on bedside chart Check record of fluid intake and output and body weight Check results of fractional urine tests for glucose and acetone Check results of biochemical blood tests, especially determinations of glucose, inorganic phosphorus, and electrolyte levels Examine dressing covering site of infusion Read progress notes to maintain familiarity with patient's course, results of studies. and proposed plan Make appropriate notes in chart to keep nursing and medical staff informed about nutritional progress Table 4. Substances to be monitored in plasma or serum of patients receiving total parenteral nutrition SMA 6/60 test BUN Carbon dioxide Chio ride Glucose Potassium ,Sodium
SMA 12/60 test Album in Alkaline phosphatase Bilirubin Calcium Cholesterol Creatine phosphokinase
vein. The patient is placed in the Trendelenburg position with a rolled sheet between the scapulae to allow the shoulders to fall backward. The proposed puncture site is at the mid point of and about 1 to 2 cm below the clavicle. This area of skin is defatted with acetone and scrubbed for five minutes with an iodine solution, such as povidoneiodine (Betadine). During these preliminaries the operator reassures the patient, ex plains the procedure, and gives instruction in how to perform the Valsalva maneuver. The selected puncture site is anesthetized. The opera tor then places one finger in the suprasternal notch, punctures the skin with a needle on a syringe, and directs the needle taward the no teh, turning the bevel to174
Creatinine Lactic dehydrogenase Phosphorus SGOT Total protein Urie ac id
ward the patient's heart. When the needle bas been advanced slightly the patient is asked to perform the Valsalva maneuver; the subclavian vein is then punctured. As saon as blood flows into the syringe the operator grasps the needie with a hemostat, removes the syringe, and inserts the catheter, carefully threading it into the superior vena cava. Once the catheter is inserted to its hub, bath needle and catheter are slowly withdrawn until the needle can be removed. An infusion of isotonie saline or glucose solution is begun, the catheter is sutured to the skin, the area is carefully cleaned with povidone-iodine solution and alcohol, and a small a mount of povidone-iodine ointment is placed around the puncture
site. The area is covered with a sterile gauze sponge and the surrounding skin is sprayed with tincture of benzain and allowed to dry. A rectangle of semipermeable dressing, such as Elastoplast, is placed over the site. Only the edges are taped, th us permitting perspiration to evapora te through the central area. Infusion of isotonie solution is continued until an x-ray film confirms that the tip of the catheter is 1 to 2 cm above the right auricle. The hypertonie TPN solution is then connected to an in-line filter which, in turn, is connected to the catheter, and the junction is carefully taped.J7 The TPN solution will flow by gravity through a 0.45 J.L filter; if a constant flow rate is essential, a pump must be used.3 8 Monitoring The most effective way to monitor TPN therapy is to establish a team consisting of a special nurse, a pharmacist, and a physician. At !east one member of the team should visit the patient daily. The points to be checked are shawn in table 3. The team nurse supervises a change of dressing three times weekly. The same strict asepsis must be used as for catheter insertion.3 9
Laboratory monitoring-Urine should be collected four times daily at about six-hour intervals and each fraction tested for glucose and acetone. Results can be recorded conveniently on the same form as that used for diabetic patients. In most patients on! y small amounts of gluVOL 65/NO 3/MARCH 1979/POSTGRAOUATE MEDICINE
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After catheter insertion, an isotonie solution should be infused until an x-ray film verifies catheter position. Infusion of TPN solution then can be started.
cose will be found in the urine and then only for one to three da ys. Transient glycosuria may occur on initiation of TPN or when the dosage is increased. The blood glucose leve! is used to identify patients who have an abnormal renal threshold for glucose. Ordinarily, such patients do not need exogenous insulin, but if glycosuria persists (3+ to 4+) and the glucose leve! is in excess of 300 mg/ dl, insulin probably will be needed. We prefer to give Regular insulin in fixed rather than "sliding scale" doses because the method used to determine the latter is imprecise and therapy is often ineffective. We do not add insulin to the infusion fluid because the subcutaneous route is more dependable. Biachemica/ tests-The SMA 6/60and SMA 12/60tests(orequivalent tests) are very useful for monitoring patients receiving TPN (table 4). Aberrations in electrolyte levels may occur in patients who Jose large quantities of fluid as a result of gastric suction, diarrhea, or drainage from a fistula. We advise against late addition of electrolytes to the TPN solution and prefer to give the necessary supplements through a peripheral vein. Knowledge of blood glucose leve! is most important early in therapy, and th us the leve! should be checked daily for severa! days until it is stable, and then twice weekly. The S MA 12/60 test gives vital information and should be performed twice VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
a week initially, then once weekly. The BUN 1creatinine ratio is normany in the range of 10 to 20. A value below 10 may mean that insufficient protein is being given. A value above 20 may reflect either excessive protein intake or bleeding into the upper digestive tract. A CBC should be performed once each week. In anemie patients, total iron-binding capacity and levels of
serum iron, folate, and vitamin B12 should also be measured. Since TPN solutions do not contain appreciable amounts of iron, it may be necessary to give iron dextran injection (lmferon) either intramuscularly or intravenously. Few emaciated patients have sufficient muscle tissue to permit use of the intramuscular route. The initial intravenous dose should be only 25 mg, given slowly. continued
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During TPN therapy, urine must be monitored for glucose and acetone and blood for changes in electrolyte levels. A CBC should be done once a week. lntravenous fat emulsion should be given in a peripheral vein to patients who must receive TPN continuously for several weeks.
Figure 1. Oxidative metabolism of glucose.
This can be repeated on subsequent days untillOO mg has been given. Under no circumstances should iron be added to the TPN solution, because of incompatibility with other components. Since TPN solutions also lack vitamin K, prothrombin and partial thromboplastin times should be measured at regular intervals. If these tests indicate a need for vi tamin K, 10 mg of an injectable preparation, eg, AquaMephyton, can be given either intramuscularly or intravenously. Essential fatty acid deficiency develops in patients who receive TPN continuously for severa! weeks.40 It can be prevented by giving intrave178
nous fat emulsion (Intralipid) in a peripheral vein.at a rate of lOO ml/hr for a dosage of 500 ml/ day. This supplies an additional 550 kcal as weil. Deficiency of trace minerais, especially of zinc and copper,4t probably develops in most patients who receive TPN for periods longer than one month. At present there is no approved IV preparation for trace minerais, but several clinics have prepared supplements that apparently meet this need. Complications
Mechanical-The most common mechanical complication of TPN is pneumothorax, but any intratho-
racic structure within reach of the needle can be damaged. The catheter may injure the right auricle or the pericardium. Thrombosis of a venous structure is always a risk, albeit small. Accidentai cutting of the catheter by the sharp needle can resuit in catheter embolization. Metabo/ic-Hyperglycemia may result from too rapid infusion of TPN solution or from administration of a too-large dose of glucose to a starved patient who has not had time to adapt.42.43 Severe hyperglycemia may result in hyperosmolar coma. If TPN is stopped abruptly, hypoglycemia may ensue as a result of endogenous secretion of insulin. This usually occurs after sudden slowing of an infusion that bas been running at a rapid rate, and it emphasizes the need for a constant flow rate. Sorne degree of hypophosphatemia occurs whenever a large amount of carbohydrate is being metabolized. Normally the two molecules of phosphate that phosphorylate each molecule of glucose are recycled by the liver and homeostasis is maintained (figure 1),44,45 With continuous infusion of glucose, the demand for phosphate persists but the sustained insulin response prevents the normal recycling of phosphate. The result is hypophosphatemia accompanied by a falling level of 2,3-diphosphoglycerate in the RBCs, causing a shift to the left in the oxygen dissociation curve of hemoglobin and resulting in tissue hypoxia. Other effects of hypophosVOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
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Pneumothorax is the most common mechan· ical complication ofTPN.
phatemia include impairment of coagulation and phagocytosis and increased rigidity of RBC walls. Hypophosphatemia occurs chiefly in patients who have been starved before initiation of TPN. If aluminum hydroxide gel has been given orally, phosphate levels may have become depleted. Measure-· ment of the serum phosphorus leve! usually is diagnostic. Treatment must be prompt: The hypertonie infusion should be replaced by a solution of 5% dextrose and 0.9% saline to which 20 mEq of phosphate per liter has been added. This solution is given at a rate of 1 liter 112 hr; response should occur within 12 to 24 hours. As soon as the serum phosphorus leve! retums to normal, TPN can be resumed, first at a reduced rate and then at the normal rate. Infection-By far the most cornmon complication of TPN therapy is infection of the IV catheter.46-49 This results from two factors: ( 1) The indwelling catheter is a foreign body that soon becomes coated with a fibrin sheath, and (2) the TPN solution is an excellent culture medium that supports growth of bacteria and fungi. The incidence of primary infection can be reduced to less than 3% if a strict protocol is followed; incidence may rise to grea ter than 50% if no protocol is used. Fever in a patient receiving TPN presents a dilemma. The risk of permitting an infected line to remain in place is considerable, but removal of the line is undesirable. We have used the following protocol when VOL 65/NO 3/MARCH 1979/POSTGRADUATE MEDICINE
the temperature exceeds 100 F (38.4 C). 1. TPN solution, IV tubing, and filter are replaced, but the catheter is left in place and TPN is continued. 2. Three blood cultures are obtained at the peak of the febrile spikes during the next 24 hours. 3. Other sources of infection are sought: nose, throat, ears, sin uses, lungs, abdomen, urinary tract. 4. If fever continues and the cause is still obscure after 24 hours, the TPN catheter is assumed to be infected. Blood for culture is taken through the catheter, the catheter is removed, and the tip is cultured for bacteria and fungi. Usually TPN can be restarted immediately in the subclavian vein on the opposite side. In patients who have frequent episodes of bacteremia, such as those with burns, disseminated neoplasms, or multiple intraabdominal abscesses, it may be necessary to replace the catheter twice a week. Termination of TPN The decision to stop TPN may be based on an adverse reaction or on correction of the factors that dictated the need for therap . It is advisable that the rate of flow of the infusion be reduced for 24 hours before removal of the catheter and that a peripheral infusion of 10% dextrose in water, !liter in 12 hours, be given subsequently (under the assumption that the patient has begun to eat and can take feedings at intervals in the event of hypoglycemie symptoms).
Conclusion Total parenteral nutrition (TPN) is a potent form of therapy. It is particularly useful in patients who must undergo surgery or those with conditions that preclude normal feeding. The procedure is not without risk, but better understanding of the basic principles involved, refinements in technique, and experience with its use in different situations have combined to improve the results of therapy over those fmt obtained. TPN represents an important therapeutic advance and emphasizes the need for an understanding of nutritional principles by physicians and for a team approach to the management of complicated conditions. Address reprint requests to Robert E. Hodges, MD, Department of Internai Medicine, Section of Nutrition, University of California School of Medicine, Davis, CA 95616. References 1. Cuthbertson DP: Further observations on the disturbance of metabolism caused by injury, with particular reference to the dietary requirements of fracture cases. Br J Surg 23:505, 1936 2. Munro H: Basic concepts in the use of amino acids and protein hydrolysates for parenteral nutrition. IV. Additive review. Drug Intell Clin Pharm 6:216, 1972 3. Meng HC: Use of fat emulsions in parenteral nutrition. Drug Intell Clin Pharm 6:321, 1972 4. Dudrick SJ, Wilmore DW, Vars HM, et al: Long-term parenteral nutrition with growth, development and positive nitrogen balance. Surgery64:134,1968 S. Dudrick SJ, Wilmore DW, Vars HM, et al: Can intravenous feeding as the sole means of nutrition support growth in the child and re-
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store weight Joss in an adult? An affirmative answer. Ann Surg 169:974, 1969 6. Cahil GF Jr, Felig P, Marliss EB: Sorne physiologie princip les of parenteral nutrition. In Fox CL, Nahas GG (Editors): Body Fluid Replacement in the Surgical Patient. New York, Grune & Stratton Inc, 1970, p 286 7. Vinnars E, Fürst P, Hermansson IL, et al: Protein catabolism in the postoperative state and its treatment with amino acid solutions. Acta Chir Scand 136:95, 1970 8. Hinton P, Allison SP, Littlejohn S, et al: Insulin and glucose to reduce catabolic response to injury in burned patients. Lancet 1:767, 1971 9. Turner FP: Intravenous hyperalimentation. (Letter) JAMA 223:441, 1973 10. Intravenous feeding. (Editorial) Lance! 2:1179, 1973 11. Dudrick SJ, Rhoads JE: New horizons for intravenous feeding. JAMA 215:939, 1971 12. Dudrick SJ, Ruberg RL: Principles and practice of parenteral nutrition. Gastroenterology 61:901, 1971 13. Meng HC: Princip les of parenteral nutrition. Hosp Med, Jan 1971, p 102 14. Owings JW, Bomar WE Jr, Ramage RC: Parenteral hyperalimentation and its practi-. cal applications. Ann Surg 175:712, 1972 15. Hutson DG, Zeppa R: Sorne observations on the use of parenteral alimentation. South Med J 65:583, 1972 16. Parsa MH, Habif DV, Ferrer JM, et al: Intravenous hyperalimentation: Indications, technique and complications. Bull NY Acad Med 48:920, 1972 17. Heird WC, Winters RW: Total intravenous alimentation. Am J Dis Child 126:287, 1973 18. Heird WC, Winters RW: Total parenteral nutrition: The state of the art. J Pediatr 86:2, 1975 19. Abbott WM: Indications for parenteral nutrition. In Fischer JE (Editor): Total Parenteral Nutrition. Boston, Little Brown & Co, 1976, p 3 · 20. Rush BF Jr, Richardson JD, Griffin WO Jr: Positive nitrogen balance immediately after abdominal operations. Am J Surg 119:70, 1970 21. McNamara JJ, Molot MD, Wissman D, et al: Intravenous hyperalimentation: An important adjunct in the treatment of combat
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casualties. Am J Surg 122:70, 1971 22. Steiger E, Allen TR, Daly JM, et al: Beneficiai effects of immediate postoperative total parenteral nutrition. Surg Forum 22:89, 1971 23. Irving MH, Rushman GB: Parenteral nutrition for the surgical patient. Anaesthesia 26:450, 1971 24. Wilmore DW, Curreri PW, Spitzer KW, et al: Supranorrnal dietary intake in therrnally injured hypermetabolic patients. Surg Gynecol Obstet 132:881, 1971 25. Van Way CW 3d, Meng HC, Sandstead HH: An assessment of the role of parenteral alimentation in the management of surgical patients. Ann Surg 177:103, 1973 26. Hindmarsh JT, Clark RG: The effects of intravenous and intraduodenal feeding on nitrogen balance after surgery. Br J Surg 60:589, 1973 27. Dolanski EA, Stahlman MT, Meng HC: Parenteral alimentation of premature infants under 1,200 grams. South Med J 66:41, 1973 28. Lloyd-Still JD, Shwachman H, Filler RM: Protracted diarrhea of infancy treated by intravenous alimentation. 1. Clinical results of 16 infants. Am J Dis Child 125:358, 1973 29. Popp MB, Law EJ, MacMillian BG: Parenteral nutrition in the burned child: A study oftwenty-six patients. Ann Surg 179:219, 1974 30. Lloyd-Still JD, Shwachman H, Filler RM: Intravenous hyperalimentation in pediatries. AmJ Dig Dis 17:1043, 1972• 31. Scribner BH, Cole JJ, Christopher TG, et al: Long-term total parenteral nutrition: The concept of an artificial gut. JAMA 212:457, 1970 32. MacFadyen BV Jr, Dudrick SJ, Ruberg RL: Management of gastrointestinal fistulas with parenteral hyperalimentation. Surgery 74:100, 1973 33. Vogel CM, Corwin TR, Baue AE: Intravenous hyperalimentation in the treatment of inflammatory diseases of the bowel. Arch Surg 108:460, 1974 34. Reilly J, Ryan JA, Strole W, et al: Hyperalimentation in inflammatory bowel disease. AmJSurg 131:192,1976 35. Greene HL: Vitamins in total parenteral nutrition. Drug lntell Clin Pharm 6:355, 1972 36. Dudrick SJ, Wilmore DW: Long-terrn parenteral feeding. Hosp Prac 3:65, 1968
37. Wilmore DW, Dudrick SJ: An in-tine filter for intravenous solutions. Arch Surg 99:462, 1969 38. Monohan JJ, Webb JW: lntravenous infusion pumps: An added dimension toparenteral therapy. Am J Hosp Pharrn 29:54, 1972 39. Parsa MH, Thomton BH, Ferrer JM: Central venous alimentation. Am J Nurs 72:2042, 1972 40. Fleming CR, Smith LM, Hodges RE: Essential fatty acid deficiency in adults receiving total parenteral nutrition. Am J Clin Nutr 29:976, 1976 41. Fleming CR, Hodges RE, Hurley LS: A prospective study of serum copper and zinc Ievels in patients receiving total parenteral nutrition. Am J Clin Nutr 29:70, 1976 42. Danowski TS, Nabarro JD: Hyperosmolar and other types of nonketoacidotic coma in diabetes. Diabetes 14:162, 1965 43. Dudrick SJ, MacFadyen BV Jr, Van Buren CT, et al: Parenteral hyperalimentation: Metabolic problems and solutions. Ann Surg 176:259, 1972 44. Silvis SE, Paragas PD Jr: Fatal hyperalimentation syndrome: Animal studies. J Lab Clin Med 78:918, 1971 45. Silvis SE, Paragas PD Jr: Paresthesias, weakness, seizures, and hypophosphatemia in patients receiving hyperalimentation. Gastroenterology 62:513, 1972 46. Ashcraft KW, Leape LL: Candida sepsis complicating parenteral feeding. JAMA 212:454, 1970 47. Boeckman CR, Krill CE Jr: Bacterial and fungal infections complicating parenteral alimentation in infants and children. J Pediatr Surg5:117, 1970 48. Goldmann DA, Maki DG, Rhame FS, et al: Guidelines for infection control in intravenous therapy. Ann Intern Med 79:848, 1973 49. Maki DG, Goldmann DA, Rhame FS: Infection control in intravenous therapy. Ann Intern Med 79:867, 1973
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