World J. Surg., 2, 215-222, 1978
Nutritional Support of Burn Patients P. William Curreri, M.D. Burn Center, The New York Hospital-CornellMedicalCenter, New York, New York, U.S.A.
Often these fatal complications are a manifestation of acute nutritional deficiency, and their incidence may be significantly decreased if the nutritional requirements of the patient are met during the early postburn period. Therefore, it is mandatory that physicians be aware of the nutritional requirements of the patient with massive thermal injury, and that a specific nutritional program be outlined to ensure the intake of sufficient calories and nitrogen in order to prevent prolonged negative energy balance. It has been established previously that major thermal injury is characterized by a hypermetabolic response [ 1-4]. The magnitude of the increase in resting metabolic expenditure is proportional to the size of the thermal injury and may reach a level of 150200% of normal. Such hypermetabolism is associated with markedly increased energy requirements.
Major thermal injury is characterized by a hypermetabolic response. Failure to provide burn patients with sufficient exogenous caloric and nitrogen intake results in pronounced weight loss, impaired wound healing, decreased host resistance to infection, and cellular dysfunction. Nutritional therapy should be directed at environmental control, prevention of infection, early wound closure, progressive physical activity, and the provision of sufficient exogenous calories and nitrogen to prevent unnecessary catabolic seque|ae. During the past 10 years, new methods have emerged for providing better nutrition to severely burned patients. As a result, morbid complications of prolonged catabolism have been significantly reduced, and survival of patients with major thermal injury has been markedly enhanced.
The mortality rate associated with serious thermal injury has been markedly reduced over the past 25 years. In part, the increased survival of severely burned patients is related to improved diagnostic and therapeutic modalities for the treatment of postburn hypovolemic shock and pulmonary dysfunction. In addition, the utilization of physiological dressings to achieve wound closure and the development of specialized burn teams, incorporating the expertise of specialized medical and paramedical personnel, have been associated with decreased morbidity in the hospitalized patient population of major burn centers. Nevertheless, late deaths occurring 3 to 6 weeks following burn injury are not uncommon as a result of septic complications or failure of wound healing.
Clinical M a n a g e m e n t
Nutritional management of the patient with major thermal injury requires that considerable effort be expended to assure optimum conditions in 5 principal areas: (a) control of external environment; (b) prevention of septic complications; (c) expeditious wound debridement and closure with heterograft, homograft, and autograft; (d) early institution of active physical therapy; and (e) provision of exogenous caloric intake of sufficient magnitude to prevent prolonged negative energy balance. Cold stress potentiates the hypermetabolic response associated with thermal injury [5, 6]. Ambient temperatures below 25~ are associated with
Supported by Grant No. GM21748-03 from the National Institutes of Health. Reprint requests: P. William Curreri, M.D., 525 East 68th Street, Room F-758, New York, New York 10021, U.S.A.
0364-2313/78/0002-215 $01.60 9 1978 Socirt6 Internationale de Chirurgie
215
216
increased levels of circulating catecholamines and with the onset of shivering. An external environment in excess of 28~ is necessary to minimize that part of metabolic expenditure associated with heat production and maintenance of core temperature. Experimental observations at the U.S. Army Institute of Surgical Research suggest that burned patients who are allowed to control their own ambient environment usually noted maximal comfort at a temperature of 30~ [7]. Although it is often impractical to maintain an exceptionally warm environment within the entire burn unit, the ambient temperature of each individual patient may be modified by the use of a suspended Apollo heat shield (Fig. 1) which radiates dry heat over the exposed surfaces of the patient without significantly altering the ambient temperature in the rest of the room. Apprehension and pain also stimulate an exaggerated metabolic response and potentiate catecholamine secretion. The judicious administration of appropriate narcotics and tranquilizers to minimize
Fig. 1. Apollo Heat Shield suspended over bed utilized exclusively for patients with major thermal bums. Radiant heat is directed onto each individual patient. The Shield provides maximal comfort for the patient while only minimally elevating the ambient temperature in the surrounding work space.
World J. Surg. Vol. 2, No. 2, March, 1978
patient discomfort should be employed to reduce metabolic expenditure associated with painful procedures performed within the burn unit. Many investigators [8, 9] have confirmed the hypermetabolic response to pulmonary or bum wound septic complications. The utilization of topical chemotherapeutic agents in the United States has markedly decreased the incidence of burn wound sepsis in patients with major injury. Moreover, regular monitoring of the burn wound with quantitative biopsy cultures, as described by Loebl [10, 11], has provided a rapid diagnosis of excessive bacterial proliferation within full-thickness bums. The administration of specific antimicrobial agents delivered by subeschar clysis has been utilized to avert systemic sepsis in such patients [ 12]. As a consequence, death from bum wound sepsis has been markedly reduced during the past decade. However, unsuccessfully treated septic complications not only increase metaboric expenditure, but often interfere with the gastrointestinal delivery of enough exogenous calories to meet nutritional needs, since carbohydrate intolerance and paralytic ileus frequently are associated with recurrent episodes of septicemia. Prolonged negative energy balance results in the excessive utilization of endogenous fat and protein for energy needs. A marked decrease in lean muscle mass often results in diminished ability to perform kinetic work. The maintenance or replacement of muscle mass is dependent on the administration of sufficient exogenous calories and nitrogen for substrate utilization, as well as active therapy to promote muscle hypertrophy. Therefore, the early institution of a complete physical therapy program, designed not only to maintain range of joint motion, but also to prevent muscle atrophy, is an integral part of any nutritional program. Spontaneous conversion from a catabolic to an anabolic state is usually not observed in severely burned patients until burn wound closure with autograft has been accomplished, unless supernormal diets are administered [ 13, 14]. Thus, if wound closure is not promptly achieved after development of suitable granulation tissue, an unnecessarily increased requirement for exogenous calories is likely to exist for many weeks following burn injury. Obviously, the cornerstone of nutritional management is the provision of enough exogenous calories and nitrogen to prevent prolonged catabolism following a major burn. Whenever possible, the gastrointestinal tract should be utilized for the administration of dietary programs designed to supply the total nutritional needs of the patient during postburn convalescence in the hospital. The actual caloric requirements depend not only on body size or body surface area, but also on the magnitude of bum injury. Estimates of daily energy expenditure (caloric
P.W. Curreri: Nutritional Support of Burn Patients
requirement) in adults with major thermal injury may be calculated by the formula: 25 kcal/kg body weight plus 40 kcal/% total body surface burn [ 15]. Children under the age of 8 require approximately 60 kcal/kg body weight plus 35 kcal/% total body surface burn. Maintenance of adequate nutrition is more appropriately monitored by accurate daily measurements of body weight. Immediately postburn, body weight increases subsequent to fluid retention following intravenous resuscitation. However, mobilization of edema fluid occurs during the first 10 postburn days and is excreted by the 10th postburn day. Additional loss of up to 10% of preburn weight is usually well tolerated, provided the patient was not nutritionally depleted prior to his injury. On the other hand, weight loss exceeding 10% is often associated with an increased incidence of retarded epithelialization, septic complications, and multiple organ failure. Spontaneous dietary intake by the patient with a major thermal burn is frequently of insufficient quantity to provide for positive energy balance. Most individuals find it Exceedingly difficult to voluntarily consume diets which substantially exceed the preburn caloric intake with which they have become habitually accustomed. However, it is imperative that the physician establish some guidelines to ensure that the patient has reached appropriate nutritional goals in a reasonable period of time. In most cases, patients who have suffered a 10% loss of preinjury weight, or in whom it has been impossible to establish a satisfactory dietary intake which meets nutritional requirements by the 7th postburn day, should be supplemented either parenterally or enterally in order to prevent complications associated with further nutritional deficiency. In general, enteral feedings may be accomplished by the insertion of a small silastic nasogastric feeding tube through which complete diets may be efficiently delivered. In order to ensure uniform delivery rates, an infusion pump should be employed to deliver nutrients into the gastrointestinal tract (Fig. 2). The utilization of such pumps increases the volume of fluid which can be safely delivered into the stomach over a 24-hour period without substantially increasing the risk of gastric distension, vomiting, or pulmonary aspiration. Tube feeding preparations may be purchased in many different forms; thus, the physician may choose a diet which is compatible with the absorptive capabilities of the patient's gastrointestinal tract. Burn patients only rarely exhibit malabsorption syndromes and, therefore, a complete, homogenized diet is preferable, since such feeding supplements are less hyperosmolar than the more elemental dietary preparations. A caloric density of between 1 and 1.5 kcal/ml is usually well tolerated, provided the tube feedings are initially administered in small volumes
217
at a constant rate. The rate of infusion may be gradually increased as tolerance of the gastrointestinal tract is demonstrated. Although nutritional supplementation provided via the gastrointestinal tract is optimal, frequently it is necessary to provide nutritional requirements entirely or in part by parenteral means in the massively burned patient. Such patients often exhibit prolonged paralytic ileus which prevents sufficient utilization of the gastrointestinal tract to allow absorption of nutrients. Unfortunately, there is a natural inclination to procrastinate during the immediate postburn period before instituting a parenteral program. The development of a safe method for the delivery of hyperosmolar solutions directly into a central vein by Dudrick [16] has allowed the physician to maintain positive energy balance throughout the postburn period, even when enteral administration of nutrients is less than ideal. Most intravenous hyperalimentation solutions contain a carbohydrate source, usually glucose,
Fig. 2. One of many manufactured constant infusion pumps which allow uniform delivery of either intravenous or enteral preparations utilized to promote positive energy balance.
218
which is combined with a second solution containing the nitrogen source, usually crystalline amino acids. The final mixed solution of 25% glucose and between 2.5-5% amino acids contains about 1 kcal/ml. To this solution must be added appropriate minerals and vitamins in order to meet daffy requirements. Since all hypertonic nutrient solutions readily support microbiological growth, they must be prepared in the hospital pharmacy by individuals familiar with the safety precautions required for maintenance of strict aseptic technique. A clean air environment created by laminar air flow in the pharmacy preparation area is strongly recommended, and solutions should be stored at refrigerated temperatures of 5~ following preparation until ready for administration to the patient. The catabolic patient often exhibits a large total body deficit of intracellular cations and anions, as a result of prolonged utilization of endogenous tissue to meet energy requirements. The breakdown of lean tissue mass results in the liberation of the principal intracellular cations and anions (potassium, magnesium, and phosphorous) into the extracellular fluid. Subsequent renal clearance results in progressive total body deficits of these minerals, even though plasma concentrations may remain relatively normal. Later, when the patient has been converted to an anabolic state by the provision of additional exogenous calories, new cells are again synthesized and, unless the intracellular anions and cations are simultaneously administered, serious extracellular and plasma hypokalemia, hypomagnesemia, and hypophosphatemia results. The delivery of hypertonic solutions into a peripheral vein of small diameter results in rapid development of chemical phlebitis. To avoid this complication, hyperosmotic fluids must be delivered into central veins, e.g., the subclavian, where there is sufficient blood flow to ensure rapid dilution of the solution. It is mandatory that the delivery rate of the solutions remains constant over a 24-hour period and that the initial rate of administration be slow enough to avoid hyperglycemia. In general, most patients tolerate between 1,200-1,800 ml during the first 24 hours without evidence of glucosuria. Thereafter, the rate of delivery may be slowly increased each day until the desired caloric intake is reached. Should significant glucosuria be noted as the daily volume of fluid is increased, the administered volume should be held at a constant level for several days to allow the patient to respond with increased endogenous insulin output. The sudden development of hyperglycemia or glucosuria in a patient who has previously tolerated a specific daily volume of hyperosmotic nutrient fluid suggests a septic complication with secondary carbohydrate intolerance. Central catheters must be introduced into central
World J. Surg. Vol. 2, No. 2, March, 1978
veins utilizing strict aseptic technique. The skin should be surgically prepared with an acceptable antimicrobial soap for a period of 10 minutes. Personnel should utilize caps, masks, and gloves to prevent inadvertent contamination of the catheter. In most cases, fluid should be delivered by infusion pumps to prevent serious alterations in the rate of delivery. Solutions should be prepared in volumes small enough to ensure that the solution bottle will not be exposed to room temperature for more than I2 hours. Tubing between the solution and the catheter is changed every 24 hours in order to minimize bacterial colonization. The catheters within the central vein should be removed at 3-day intervals and reinserted in an alternative site, since the occurrence of septic thrombophlebitis within central veins is not infrequent in the thermally injured patient, in whom indwelling central vein catheters are left for longer periods of time. Patients with major thermal burns must be carefully monitored during the administration of hypertonic nutrient solutions. Fractional urines should be obtained at least every 6 hours and blood sugar, serum electrolytes, and arterial blood gasses should be obtained daily until the patient has reached the desired caloric intake. In addition, body weight and fluid balance should be carefully reviewed on a daily basis. A complete blood count, prothrombin time, creatinine, SGOT, serum alkaline phosphatase, serum magnesium, and serum phosphorous should be periodically assayed several times a week. Adjustments in the mineral and vitamin contents of the solutions will be required after review of the patient response. It is important to note that iron, vitamin B12, and folic acid are incompatible or unstable with most hyperosmotic solutions and must be provided by a separate parenteral or enteral route to prevent long-term deficiencies. Complications of intravenous hyperalimentation are most easily divided into 3 specific areas, namely, anatomical, septic, and physiological. Anatomical complications resulting from faulty insertion of the catheter have included pneumothorax, hemothorax, hydrothorax, catheter perforation of the right atrium, arterial and venous thrombosis, and catheter embolism. These complications are best prevented by scrupulously observing established techniques for insertion of central venous catheters. Septic complications may be minimized by scrupulously observing aseptic techniques during preparation and delivery of solutions. If clinical signs of sepsis appear, the bottle containing the solution should be immediately removed and a freshly prepared solution bottle utilized as a replacement. The suspect solution should be returned to the pharmacy for appropriate bacteriological and fungal culture, as well as for pyrogen analysis. Should clinical signs of
P.W. Curreri: Nutritional Support of Burn Patients
sepsis not disappear following this simple maneuver, the catheter itself should be immediately removed and a new catheter inserted in the central vein. In order to prevent infection of the catheter tip from the skin, the catheter should always be kept in an occlusive dressing, which is changed at least every 24 hours, at which time the skin around the catheter is surgically scrubbed with an appropriate antibiotic soap solution. Numerous physiological complications have been reported as a result of inappropriate administration of hyperalimentation solutions. Most common is the presence of hyperglycemia, glycosuria, osmotic diuresis, and dehydration. This complication usually results when the rate of infusion has been too rapidly increased in massively burned patients or patients with major secondary infection. Such patients may have extraordinarily high levels of catecholamine release, as well as moderate hepatic dysfunction resulting in carbohydrate intolerance. Usually a reduction in the rate of administration, as well as small supplemental doses of insulin, will correct this complication. Hypokalemia, hypophosphotemia, and hypomagnesemia will result when inadequate concentrations of these minerals are added to the solutions. In addition, hypercalcemia is occasionally observed when insufficient inorganic phosphate has been administered. Occasionally, congestive heart failure or pulmonary edema have resulted from excessively rapid infusion of hypertonic solutions, particularly in elderly individuals with previous cardiac insufficiency. Rarely, anemia will be noted in patients in whom insufficient folic acid, vitamin B12, or iron has been administered, either by enteral means or by a separate parenteral route. Patients receiving only parenteral nutrition with carbohydrate and amino acids may develop essential fatty acid (EFA) deficiency. This syndrome is clinically recognized by the development of scaly lesions of the skin and by a progressive loss of hair. Confirmation of EFA deficiency may be ascertained by measurement of the triene:tetraene ratio of total serum fatty acids [17]. A simultaneous increase in plasma eicosatrienoic acid is usually observed. EFA deficiency is most easily avoided by including small amounts of fat administered via the gastrointestinal tract. If the gastrointestinal tract cannot be utilized, essential fatty acid deficiency must be treated by intravenous administration of small amounts of fat emulsion. The intravenous administration of fat emulsions and amino acid solutions by peripheral vein may also be used to supplement enteral caloric intake. However, total nutritional support via a peripheral vein is rarely possible, since the caloric requirements are so markedly elevated in patients with major thermal injury. Furthermore, it has been shown recently that the delivery of carbohydrate
219 Table 1. Body composition of normal man (70 kg).
Substrate
Weight (kg)
Kcal.
Water and Minerals Carbohydrates Protein Fat Total
48.7 0.3 6.0 15.0 70.0
0 1,200 25,000 140.000 166,000
calories to thermally injured patients results in increased protein-sparing when compared to isocaloric administration of fat emulsions [ 18].
Clinical Malnutrition in the Burn Patient
The body composkion of a normal 70 kg male is tabulated in Table 1. Total oxidation of tissue in such an individual would yield approximately 166,000 kcal. Healthy individuals cannot tolerate acute weight loss of more than one-third lean body weight. Thus, an extensively burned adult, with energy requirements of 5,000 kcal/day, becomes a severe nutritional risk in approximately 11 days, assuming no caloric intake. Nutritional deficiency, resulting in death, may be insidious and masquerade in many clinical forms. However, since most of the kinetic energy requirements of the supine, bedridden patient are associated with maintenance of normal respiratory function, the most common cause of death in postburn patients with acute malnutrition is pulmonary sepsis. An ineffective respiratory effort results in progressive atelectasis with subsequent lung infection by opportunistic pathogens. Weight loss inevitably occurs in patients with major thermal injury unless extraordinary means are taken to provide sufficient exogenous calories to prevent prolonged negative energy balance. In a retrospective study, the U.S. Army Institute of Surgical Research noted an average weight loss of more than 25% of the preburn weight within the first 8 postburn weeks in patients with greater than 40% total body surface burns [19]. These extraordinary examples of acute weight loss occurred despite energetic attempts to provide the patients with high caloric meals as well as interval nutritional supplements. Voluntary intake of calories rarely exceeded preburn habitual caloric intake, even in the most cooperative patients. Profound weight loss is often associated with delayed reepithelialization of second degree burn wounds and the development of unhealthy granulation tissue in areas of third degree burns. In addition, the superior mesenteric artery syndrome has been reported in patients following pronounced weight
220
loss [20]. This syndrome presents itself as a functional obstruction of the third portion of the duodenum and occurs coincident with the loss of fat in the retroperitoneum, with subsequent narrowing of the angle between the aorta and the superior mesenteric artery, through which the duodenum passes. Patients with acute malnutrition may exhibit decreased immunological function. Alexander [21] has suggested that the ability of the neutrophil to kill bacteria following phagocytosis is dependent on caloric intake. In addition, Law et al. [22] have shown that T-cell function is markedly depressed in animals following calorie-nitrogen malnutrition. In addition to these unfavorable physiological consequences of malnutrition, it has recently been demonstrated that the cellular metabolism of erythrocytes, isolated from severely burned patients maintained in negative energy balance for more than a week, is severely impaired [23]. Significant elevation of red blood cell intracellular sodium concentration is observed in these patients, whereas normal concentrations of intracellular sodium are maintained in those patients receiving enough exogenous calories to meet their nutritional needs. Analysis of erythrocyte transmembrane sodium efflux and influx in malnourished burn patients revealed that the increased intracellular sodium concentration resulted from severe inhibition of the active transport (sodium pump) mechanism. Thus, the metabolic performance of erythrocytes from malnourished, thermally injured patients, mimics the sick cell syndrome observed in dying organs. The sodium pump defect could be reversed within 72 hours when adequate exogenous caloric intake was reinstituted. Similar changes have been demonstrated in uninjured muscle of rats following burn injury (40% total body surface) and 20-30% acute weight loss.
R6sum6
Toute br01ure grave augmente le m6tabolisme. Si l'on ne fournit pas au patient un apport calorique et azot6 stfffisant, on voit apparaitre une perte de poids, des troubles de cicatrisation, une diminution de la r6sistance h l'infection et des perturbations au niveau cellulaire. La th6rapeutique nutritionnelle doit viser ~t contr61er l'environnement, pr6venir l'infection, faciliter la cicatrisation des plaies, accroitre l'activit6 physique, apporter suffisamment de calories et d'azote pour pr6venir les cons6quences de l'hypercatabolisme. Les nouvelles th6rapeutiques mises au point au cours des 10 derni6res ann6es ont am61ior6 la nutrition des br016s graves. Les complications du catabolisme prolong6 ont donc 6t6 r6duites et la survie est am61ior6e.
World J. Surg. Vol. 2, No. 2, March, 1978
References
1. Cuthbertson, D.P.: The disturbance of metabolism produced by bony and nonbony injuries. Biochem. J. 24:1244, 1930 2. Cuthbertson, D.P.: Observation on disturbances of metabolism produced by injury to the limbs. Quart. J. Med. 25:233, 1932 3. Roe, C.F., Kinney, J.M.: The caloric equivalent of fever: influence of major trauma. Ann. Surg. 161:140, 1965 4. Kinney, J.M.: Calories: nitrogen: disease and injury relationships. In Total Parenteral Nutrition. Acton, Mass., Publishing Sciences Group, Inc., 1974, pp. 8191 5. Wilmore, D.W., Long, J.M., Mason, A.D., Jr., Skreen, R.W., Pruitt, B.A., Jr.: Catecholamines: mediator of the hypermetabolic response to thermal injury. Ann. Surg. 186:53, 1974 6. Wilmore, D.W.: Nutrition and metabolism following thermal injury. Clin. Hast. Surg. 1:603, 1974 7. Wilmore, D.W., Orcutt, T.W., Mason, A.D., Jr., Pruitt, B.A., Jr.: Alterations in hypothalamic function following thermal injury. J. Trauma /5:697, 1975 8. Bradham, G.B.: Direct measurement of total metabolism of a burned patient. Arch. Surg. 105:410, 1972 9. Roe, C.F.: Temperature regulation and energy metabolism in surgical patients. Prog. Surg. 12:93, 1973 10. Loebl, E.C., Marvin, J.A., Heck, E.L., Curreri, P.W., Baxter, C.R.: The use of quantitative biopsy cultures in bacteriologic monitoring of burn patients. J. Surg. Res. 16:1, 1974 11. Loebl, E.C., Marvin, J.A., Heck, E.L., Curreri, P.W., Baxter, C.R.: The method of quantitative burn wound biopsy cultures and its routine use in the care of the burned patient. Am. J. Clin. Pathol. 61:20, 1974 12. Curreri, P.W., Marvin, J.A.: Advances in the clinical care of burned patients. West. J. Med. 123:275, 1975 13. Wilmore, D.W., Curreri, P.W., Spitzer, K.W., Spitzer, M.E., Pruitt, B.A., Jr.: Supernormal dietary intake in thermally injured hypermetabolic patients. Surg. Gynecol. Obstet. 132:881, 1971 14. Curreri, P.W.: A long-term supernormal caloric dietary program in extensively burned patients. In Intravenous Hyperalimentation, G.S.N. Cowan, Jr., W.L. Scheetz, editors. Philadelphia, Lea and Febiger, 1972, pp. 136-141 15. Curreri, P.W., Richmond, D., Marvin, J.A., Baxter, C.R.: Dietary requirements of patients with major burns. J. Am. Diet. Assoc. 65:415, 1974 16. Dudrick, S.J., Wilmore, D.W., Vats, H.M.: Longterm total parenteral nutrition with growth, development, and positive nitrogen balance. Surgery 64:134, 1968 17. Meng, H.C.: Fat emulsions. In Total Parenteral Nutrition. Acton, Mass., Publishing Science Group, Inc., 1974, pp. 178-179 18. Long, J.M., Wilmore, D.W., Mason, A.D., Jr., Pruitt, B.A., Jr.: Comparison of carbohydrate and fat as caloric sources. Surg. Forum 26:108, 1975 19. Newsome, T.W., Mason, A.D., Jr., Pruitt, B.A., Jr.: Weight loss following thermal injury. Ann. Surg. 178:215, 1973 20. Reckler, J.M., Bruck, H.M., Munster, A.M., Curreri, P.W., Pruitt, B.A., Jr.: Superior mesenteric artery
P.W. Curreri: Nutritional Support of Burn Patients
syndrome as a consequence of burn injury. J. Trauma 12:979, 1972 21. Alexander, J.W.: Emerging concepts in the control of surgical infections. Surgery 75:934, 1974 22. Law, D.K., Dudrick, S.J., Abdau, N.I.: The effects of protein caloric malnutrition on immune competence of
221
the surgical patient. Surg. Gynecol. Obstet. 139:257, 1974 23. Curreri, P.W., Hicks, J.E., Aronoff, R.J., Baxter, C.R.: Inhibition of active sodium transport in erythrocytes from burn patients. Surg. Gynecol. Obstet. 139:538, 1974.
Invited Commentary C. Francis Roe, M.D. Yale UniversitySchoolof Medicine, New Haven, Connecticut,U.S.A.
The problem of nutritional maintenance is widespread in surgical practice, and nowhere more important than in the care of severely burned patients. As Curreri points out, hypermetabolism is a major factor in such patients. The rate of energy expenditure in severely injured patients with nonthermal injuries, such as multiple long bone fractures, may be increased by up to 25% of the resting value, but severely burned patients can show a doubling of their resting rate of energy expenditure, a large increase approximately equivalent to the energy required for continuous jogging. This means that in order to keep in nutritional balance, up to 5,000 Kilocalories must be administered daily, absorbed, and converted into usable form. The very magnitude of this problem begets secondary problems. The rule-of-thumb calorie value for most of the hyperalimentation preparations, both enteral and intravenous, is 1 kcal/ml, which means that the patient has somehow to deal with a large fluid volume overload in addition to the problems of hyperosmolarity and electrolyte imbalance which are well described in Curreri's paper. How well are these calories utilized? How much nitrogen wastage continues during such hyperalimentation? What is the effect of sepsis on utilization of these exogenous calories? Although all these questions have been addressed at one time or another, satisfactory quantitative answers are needed to make nutritional support of these patients less of a haphazard undertaking. The science of burn treatment is bedecked with formulas, such as the Brooke formula, the Moore budget, and the Evans formula, to mention only a few. They have served as rough guidelines for early treatment and are still valid in situations where accurate measurements cannot be carried out. Likewise, Curreri's formula has value in estimating the broad outlines of the energy requirements of burned pa-
tients, but it must be remembered that large variations in energy requirements exist in patients who have suffered burns of similar magnitude. These variations depend on factors such as the use of occlusive dressings, the ambient temperature and humidity of the patient's environment, and the presence or absence of sepsis and fever. Thus, in institutions where such measurements can be carried out, actual measurements of energy expenditure by indirect calorimetry techniques are extremely useful as a basis for evaluating ongoing nutritional requirements. Curreri's paper admirably describes the difficulties and problems associated with attempting to provide sufficient calories to the hypermetabolic burn patient. These difficulties are substantial to say the least, ranging from problems in administering the huge caloric requirements to the impairment of wound healing and erythrocyte function resulting from inadequate nutritional support. Intravenous hyperalimentation catheters, even when inserted and maintained with all possible care, are liable to get infected, with potentially disastrous consequences. In nonburn patients, catheter sepsis is usually announced by fever, chills, and hyperglycemia associated with a diminished rate of glucose utilization. In severely burned patients, these vital indicators may be masked or mimicked by other factors directly related to the burn injury. For instance, the normal cutaneous control of body temperature by vasomotor activity and sweating is impaired in proportion to the extent and severity of the burn, with resulting poorly controlled swings in body temperature. Thus, an important indicator of catheter sepsis may be lost with a potentially lethal delay in diagnosis. The diminished ability of the depleted burn patient to handle sepsis adds to the hazards of this form of therapy. The potential benefits of intravenous hyperalimentation are so great, however, that these risks some-
Nutritional Support of Burn Patients P. William Curreri, M.D. Burn Center, The New York Hospital-CornellMedicalCenter, New York, New York, U.S.A.
Often these fatal complications are a manifestation of acute nutritional deficiency, and their incidence may be significantly decreased if the nutritional requirements of the patient are met during the early postburn period. Therefore, it is mandatory that physicians be aware of the nutritional requirements of the patient with massive thermal injury, and that a specific nutritional program be outlined to ensure the intake of sufficient calories and nitrogen in order to prevent prolonged negative energy balance. It has been established previously that major thermal injury is characterized by a hypermetabolic response [ 1-4]. The magnitude of the increase in resting metabolic expenditure is proportional to the size of the thermal injury and may reach a level of 150200% of normal. Such hypermetabolism is associated with markedly increased energy requirements.
Major thermal injury is characterized by a hypermetabolic response. Failure to provide burn patients with sufficient exogenous caloric and nitrogen intake results in pronounced weight loss, impaired wound healing, decreased host resistance to infection, and cellular dysfunction. Nutritional therapy should be directed at environmental control, prevention of infection, early wound closure, progressive physical activity, and the provision of sufficient exogenous calories and nitrogen to prevent unnecessary catabolic seque|ae. During the past 10 years, new methods have emerged for providing better nutrition to severely burned patients. As a result, morbid complications of prolonged catabolism have been significantly reduced, and survival of patients with major thermal injury has been markedly enhanced.
The mortality rate associated with serious thermal injury has been markedly reduced over the past 25 years. In part, the increased survival of severely burned patients is related to improved diagnostic and therapeutic modalities for the treatment of postburn hypovolemic shock and pulmonary dysfunction. In addition, the utilization of physiological dressings to achieve wound closure and the development of specialized burn teams, incorporating the expertise of specialized medical and paramedical personnel, have been associated with decreased morbidity in the hospitalized patient population of major burn centers. Nevertheless, late deaths occurring 3 to 6 weeks following burn injury are not uncommon as a result of septic complications or failure of wound healing.
Clinical M a n a g e m e n t
Nutritional management of the patient with major thermal injury requires that considerable effort be expended to assure optimum conditions in 5 principal areas: (a) control of external environment; (b) prevention of septic complications; (c) expeditious wound debridement and closure with heterograft, homograft, and autograft; (d) early institution of active physical therapy; and (e) provision of exogenous caloric intake of sufficient magnitude to prevent prolonged negative energy balance. Cold stress potentiates the hypermetabolic response associated with thermal injury [5, 6]. Ambient temperatures below 25~ are associated with
Supported by Grant No. GM21748-03 from the National Institutes of Health. Reprint requests: P. William Curreri, M.D., 525 East 68th Street, Room F-758, New York, New York 10021, U.S.A.
0364-2313/78/0002-215 $01.60 9 1978 Socirt6 Internationale de Chirurgie
215
216
increased levels of circulating catecholamines and with the onset of shivering. An external environment in excess of 28~ is necessary to minimize that part of metabolic expenditure associated with heat production and maintenance of core temperature. Experimental observations at the U.S. Army Institute of Surgical Research suggest that burned patients who are allowed to control their own ambient environment usually noted maximal comfort at a temperature of 30~ [7]. Although it is often impractical to maintain an exceptionally warm environment within the entire burn unit, the ambient temperature of each individual patient may be modified by the use of a suspended Apollo heat shield (Fig. 1) which radiates dry heat over the exposed surfaces of the patient without significantly altering the ambient temperature in the rest of the room. Apprehension and pain also stimulate an exaggerated metabolic response and potentiate catecholamine secretion. The judicious administration of appropriate narcotics and tranquilizers to minimize
Fig. 1. Apollo Heat Shield suspended over bed utilized exclusively for patients with major thermal bums. Radiant heat is directed onto each individual patient. The Shield provides maximal comfort for the patient while only minimally elevating the ambient temperature in the surrounding work space.
World J. Surg. Vol. 2, No. 2, March, 1978
patient discomfort should be employed to reduce metabolic expenditure associated with painful procedures performed within the burn unit. Many investigators [8, 9] have confirmed the hypermetabolic response to pulmonary or bum wound septic complications. The utilization of topical chemotherapeutic agents in the United States has markedly decreased the incidence of burn wound sepsis in patients with major injury. Moreover, regular monitoring of the burn wound with quantitative biopsy cultures, as described by Loebl [10, 11], has provided a rapid diagnosis of excessive bacterial proliferation within full-thickness bums. The administration of specific antimicrobial agents delivered by subeschar clysis has been utilized to avert systemic sepsis in such patients [ 12]. As a consequence, death from bum wound sepsis has been markedly reduced during the past decade. However, unsuccessfully treated septic complications not only increase metaboric expenditure, but often interfere with the gastrointestinal delivery of enough exogenous calories to meet nutritional needs, since carbohydrate intolerance and paralytic ileus frequently are associated with recurrent episodes of septicemia. Prolonged negative energy balance results in the excessive utilization of endogenous fat and protein for energy needs. A marked decrease in lean muscle mass often results in diminished ability to perform kinetic work. The maintenance or replacement of muscle mass is dependent on the administration of sufficient exogenous calories and nitrogen for substrate utilization, as well as active therapy to promote muscle hypertrophy. Therefore, the early institution of a complete physical therapy program, designed not only to maintain range of joint motion, but also to prevent muscle atrophy, is an integral part of any nutritional program. Spontaneous conversion from a catabolic to an anabolic state is usually not observed in severely burned patients until burn wound closure with autograft has been accomplished, unless supernormal diets are administered [ 13, 14]. Thus, if wound closure is not promptly achieved after development of suitable granulation tissue, an unnecessarily increased requirement for exogenous calories is likely to exist for many weeks following burn injury. Obviously, the cornerstone of nutritional management is the provision of enough exogenous calories and nitrogen to prevent prolonged catabolism following a major burn. Whenever possible, the gastrointestinal tract should be utilized for the administration of dietary programs designed to supply the total nutritional needs of the patient during postburn convalescence in the hospital. The actual caloric requirements depend not only on body size or body surface area, but also on the magnitude of bum injury. Estimates of daily energy expenditure (caloric
P.W. Curreri: Nutritional Support of Burn Patients
requirement) in adults with major thermal injury may be calculated by the formula: 25 kcal/kg body weight plus 40 kcal/% total body surface burn [ 15]. Children under the age of 8 require approximately 60 kcal/kg body weight plus 35 kcal/% total body surface burn. Maintenance of adequate nutrition is more appropriately monitored by accurate daily measurements of body weight. Immediately postburn, body weight increases subsequent to fluid retention following intravenous resuscitation. However, mobilization of edema fluid occurs during the first 10 postburn days and is excreted by the 10th postburn day. Additional loss of up to 10% of preburn weight is usually well tolerated, provided the patient was not nutritionally depleted prior to his injury. On the other hand, weight loss exceeding 10% is often associated with an increased incidence of retarded epithelialization, septic complications, and multiple organ failure. Spontaneous dietary intake by the patient with a major thermal burn is frequently of insufficient quantity to provide for positive energy balance. Most individuals find it Exceedingly difficult to voluntarily consume diets which substantially exceed the preburn caloric intake with which they have become habitually accustomed. However, it is imperative that the physician establish some guidelines to ensure that the patient has reached appropriate nutritional goals in a reasonable period of time. In most cases, patients who have suffered a 10% loss of preinjury weight, or in whom it has been impossible to establish a satisfactory dietary intake which meets nutritional requirements by the 7th postburn day, should be supplemented either parenterally or enterally in order to prevent complications associated with further nutritional deficiency. In general, enteral feedings may be accomplished by the insertion of a small silastic nasogastric feeding tube through which complete diets may be efficiently delivered. In order to ensure uniform delivery rates, an infusion pump should be employed to deliver nutrients into the gastrointestinal tract (Fig. 2). The utilization of such pumps increases the volume of fluid which can be safely delivered into the stomach over a 24-hour period without substantially increasing the risk of gastric distension, vomiting, or pulmonary aspiration. Tube feeding preparations may be purchased in many different forms; thus, the physician may choose a diet which is compatible with the absorptive capabilities of the patient's gastrointestinal tract. Burn patients only rarely exhibit malabsorption syndromes and, therefore, a complete, homogenized diet is preferable, since such feeding supplements are less hyperosmolar than the more elemental dietary preparations. A caloric density of between 1 and 1.5 kcal/ml is usually well tolerated, provided the tube feedings are initially administered in small volumes
217
at a constant rate. The rate of infusion may be gradually increased as tolerance of the gastrointestinal tract is demonstrated. Although nutritional supplementation provided via the gastrointestinal tract is optimal, frequently it is necessary to provide nutritional requirements entirely or in part by parenteral means in the massively burned patient. Such patients often exhibit prolonged paralytic ileus which prevents sufficient utilization of the gastrointestinal tract to allow absorption of nutrients. Unfortunately, there is a natural inclination to procrastinate during the immediate postburn period before instituting a parenteral program. The development of a safe method for the delivery of hyperosmolar solutions directly into a central vein by Dudrick [16] has allowed the physician to maintain positive energy balance throughout the postburn period, even when enteral administration of nutrients is less than ideal. Most intravenous hyperalimentation solutions contain a carbohydrate source, usually glucose,
Fig. 2. One of many manufactured constant infusion pumps which allow uniform delivery of either intravenous or enteral preparations utilized to promote positive energy balance.
218
which is combined with a second solution containing the nitrogen source, usually crystalline amino acids. The final mixed solution of 25% glucose and between 2.5-5% amino acids contains about 1 kcal/ml. To this solution must be added appropriate minerals and vitamins in order to meet daffy requirements. Since all hypertonic nutrient solutions readily support microbiological growth, they must be prepared in the hospital pharmacy by individuals familiar with the safety precautions required for maintenance of strict aseptic technique. A clean air environment created by laminar air flow in the pharmacy preparation area is strongly recommended, and solutions should be stored at refrigerated temperatures of 5~ following preparation until ready for administration to the patient. The catabolic patient often exhibits a large total body deficit of intracellular cations and anions, as a result of prolonged utilization of endogenous tissue to meet energy requirements. The breakdown of lean tissue mass results in the liberation of the principal intracellular cations and anions (potassium, magnesium, and phosphorous) into the extracellular fluid. Subsequent renal clearance results in progressive total body deficits of these minerals, even though plasma concentrations may remain relatively normal. Later, when the patient has been converted to an anabolic state by the provision of additional exogenous calories, new cells are again synthesized and, unless the intracellular anions and cations are simultaneously administered, serious extracellular and plasma hypokalemia, hypomagnesemia, and hypophosphatemia results. The delivery of hypertonic solutions into a peripheral vein of small diameter results in rapid development of chemical phlebitis. To avoid this complication, hyperosmotic fluids must be delivered into central veins, e.g., the subclavian, where there is sufficient blood flow to ensure rapid dilution of the solution. It is mandatory that the delivery rate of the solutions remains constant over a 24-hour period and that the initial rate of administration be slow enough to avoid hyperglycemia. In general, most patients tolerate between 1,200-1,800 ml during the first 24 hours without evidence of glucosuria. Thereafter, the rate of delivery may be slowly increased each day until the desired caloric intake is reached. Should significant glucosuria be noted as the daily volume of fluid is increased, the administered volume should be held at a constant level for several days to allow the patient to respond with increased endogenous insulin output. The sudden development of hyperglycemia or glucosuria in a patient who has previously tolerated a specific daily volume of hyperosmotic nutrient fluid suggests a septic complication with secondary carbohydrate intolerance. Central catheters must be introduced into central
World J. Surg. Vol. 2, No. 2, March, 1978
veins utilizing strict aseptic technique. The skin should be surgically prepared with an acceptable antimicrobial soap for a period of 10 minutes. Personnel should utilize caps, masks, and gloves to prevent inadvertent contamination of the catheter. In most cases, fluid should be delivered by infusion pumps to prevent serious alterations in the rate of delivery. Solutions should be prepared in volumes small enough to ensure that the solution bottle will not be exposed to room temperature for more than I2 hours. Tubing between the solution and the catheter is changed every 24 hours in order to minimize bacterial colonization. The catheters within the central vein should be removed at 3-day intervals and reinserted in an alternative site, since the occurrence of septic thrombophlebitis within central veins is not infrequent in the thermally injured patient, in whom indwelling central vein catheters are left for longer periods of time. Patients with major thermal burns must be carefully monitored during the administration of hypertonic nutrient solutions. Fractional urines should be obtained at least every 6 hours and blood sugar, serum electrolytes, and arterial blood gasses should be obtained daily until the patient has reached the desired caloric intake. In addition, body weight and fluid balance should be carefully reviewed on a daily basis. A complete blood count, prothrombin time, creatinine, SGOT, serum alkaline phosphatase, serum magnesium, and serum phosphorous should be periodically assayed several times a week. Adjustments in the mineral and vitamin contents of the solutions will be required after review of the patient response. It is important to note that iron, vitamin B12, and folic acid are incompatible or unstable with most hyperosmotic solutions and must be provided by a separate parenteral or enteral route to prevent long-term deficiencies. Complications of intravenous hyperalimentation are most easily divided into 3 specific areas, namely, anatomical, septic, and physiological. Anatomical complications resulting from faulty insertion of the catheter have included pneumothorax, hemothorax, hydrothorax, catheter perforation of the right atrium, arterial and venous thrombosis, and catheter embolism. These complications are best prevented by scrupulously observing established techniques for insertion of central venous catheters. Septic complications may be minimized by scrupulously observing aseptic techniques during preparation and delivery of solutions. If clinical signs of sepsis appear, the bottle containing the solution should be immediately removed and a freshly prepared solution bottle utilized as a replacement. The suspect solution should be returned to the pharmacy for appropriate bacteriological and fungal culture, as well as for pyrogen analysis. Should clinical signs of
P.W. Curreri: Nutritional Support of Burn Patients
sepsis not disappear following this simple maneuver, the catheter itself should be immediately removed and a new catheter inserted in the central vein. In order to prevent infection of the catheter tip from the skin, the catheter should always be kept in an occlusive dressing, which is changed at least every 24 hours, at which time the skin around the catheter is surgically scrubbed with an appropriate antibiotic soap solution. Numerous physiological complications have been reported as a result of inappropriate administration of hyperalimentation solutions. Most common is the presence of hyperglycemia, glycosuria, osmotic diuresis, and dehydration. This complication usually results when the rate of infusion has been too rapidly increased in massively burned patients or patients with major secondary infection. Such patients may have extraordinarily high levels of catecholamine release, as well as moderate hepatic dysfunction resulting in carbohydrate intolerance. Usually a reduction in the rate of administration, as well as small supplemental doses of insulin, will correct this complication. Hypokalemia, hypophosphotemia, and hypomagnesemia will result when inadequate concentrations of these minerals are added to the solutions. In addition, hypercalcemia is occasionally observed when insufficient inorganic phosphate has been administered. Occasionally, congestive heart failure or pulmonary edema have resulted from excessively rapid infusion of hypertonic solutions, particularly in elderly individuals with previous cardiac insufficiency. Rarely, anemia will be noted in patients in whom insufficient folic acid, vitamin B12, or iron has been administered, either by enteral means or by a separate parenteral route. Patients receiving only parenteral nutrition with carbohydrate and amino acids may develop essential fatty acid (EFA) deficiency. This syndrome is clinically recognized by the development of scaly lesions of the skin and by a progressive loss of hair. Confirmation of EFA deficiency may be ascertained by measurement of the triene:tetraene ratio of total serum fatty acids [17]. A simultaneous increase in plasma eicosatrienoic acid is usually observed. EFA deficiency is most easily avoided by including small amounts of fat administered via the gastrointestinal tract. If the gastrointestinal tract cannot be utilized, essential fatty acid deficiency must be treated by intravenous administration of small amounts of fat emulsion. The intravenous administration of fat emulsions and amino acid solutions by peripheral vein may also be used to supplement enteral caloric intake. However, total nutritional support via a peripheral vein is rarely possible, since the caloric requirements are so markedly elevated in patients with major thermal injury. Furthermore, it has been shown recently that the delivery of carbohydrate
219 Table 1. Body composition of normal man (70 kg).
Substrate
Weight (kg)
Kcal.
Water and Minerals Carbohydrates Protein Fat Total
48.7 0.3 6.0 15.0 70.0
0 1,200 25,000 140.000 166,000
calories to thermally injured patients results in increased protein-sparing when compared to isocaloric administration of fat emulsions [ 18].
Clinical Malnutrition in the Burn Patient
The body composkion of a normal 70 kg male is tabulated in Table 1. Total oxidation of tissue in such an individual would yield approximately 166,000 kcal. Healthy individuals cannot tolerate acute weight loss of more than one-third lean body weight. Thus, an extensively burned adult, with energy requirements of 5,000 kcal/day, becomes a severe nutritional risk in approximately 11 days, assuming no caloric intake. Nutritional deficiency, resulting in death, may be insidious and masquerade in many clinical forms. However, since most of the kinetic energy requirements of the supine, bedridden patient are associated with maintenance of normal respiratory function, the most common cause of death in postburn patients with acute malnutrition is pulmonary sepsis. An ineffective respiratory effort results in progressive atelectasis with subsequent lung infection by opportunistic pathogens. Weight loss inevitably occurs in patients with major thermal injury unless extraordinary means are taken to provide sufficient exogenous calories to prevent prolonged negative energy balance. In a retrospective study, the U.S. Army Institute of Surgical Research noted an average weight loss of more than 25% of the preburn weight within the first 8 postburn weeks in patients with greater than 40% total body surface burns [19]. These extraordinary examples of acute weight loss occurred despite energetic attempts to provide the patients with high caloric meals as well as interval nutritional supplements. Voluntary intake of calories rarely exceeded preburn habitual caloric intake, even in the most cooperative patients. Profound weight loss is often associated with delayed reepithelialization of second degree burn wounds and the development of unhealthy granulation tissue in areas of third degree burns. In addition, the superior mesenteric artery syndrome has been reported in patients following pronounced weight
220
loss [20]. This syndrome presents itself as a functional obstruction of the third portion of the duodenum and occurs coincident with the loss of fat in the retroperitoneum, with subsequent narrowing of the angle between the aorta and the superior mesenteric artery, through which the duodenum passes. Patients with acute malnutrition may exhibit decreased immunological function. Alexander [21] has suggested that the ability of the neutrophil to kill bacteria following phagocytosis is dependent on caloric intake. In addition, Law et al. [22] have shown that T-cell function is markedly depressed in animals following calorie-nitrogen malnutrition. In addition to these unfavorable physiological consequences of malnutrition, it has recently been demonstrated that the cellular metabolism of erythrocytes, isolated from severely burned patients maintained in negative energy balance for more than a week, is severely impaired [23]. Significant elevation of red blood cell intracellular sodium concentration is observed in these patients, whereas normal concentrations of intracellular sodium are maintained in those patients receiving enough exogenous calories to meet their nutritional needs. Analysis of erythrocyte transmembrane sodium efflux and influx in malnourished burn patients revealed that the increased intracellular sodium concentration resulted from severe inhibition of the active transport (sodium pump) mechanism. Thus, the metabolic performance of erythrocytes from malnourished, thermally injured patients, mimics the sick cell syndrome observed in dying organs. The sodium pump defect could be reversed within 72 hours when adequate exogenous caloric intake was reinstituted. Similar changes have been demonstrated in uninjured muscle of rats following burn injury (40% total body surface) and 20-30% acute weight loss.
R6sum6
Toute br01ure grave augmente le m6tabolisme. Si l'on ne fournit pas au patient un apport calorique et azot6 stfffisant, on voit apparaitre une perte de poids, des troubles de cicatrisation, une diminution de la r6sistance h l'infection et des perturbations au niveau cellulaire. La th6rapeutique nutritionnelle doit viser ~t contr61er l'environnement, pr6venir l'infection, faciliter la cicatrisation des plaies, accroitre l'activit6 physique, apporter suffisamment de calories et d'azote pour pr6venir les cons6quences de l'hypercatabolisme. Les nouvelles th6rapeutiques mises au point au cours des 10 derni6res ann6es ont am61ior6 la nutrition des br016s graves. Les complications du catabolisme prolong6 ont donc 6t6 r6duites et la survie est am61ior6e.
World J. Surg. Vol. 2, No. 2, March, 1978
References
1. Cuthbertson, D.P.: The disturbance of metabolism produced by bony and nonbony injuries. Biochem. J. 24:1244, 1930 2. Cuthbertson, D.P.: Observation on disturbances of metabolism produced by injury to the limbs. Quart. J. Med. 25:233, 1932 3. Roe, C.F., Kinney, J.M.: The caloric equivalent of fever: influence of major trauma. Ann. Surg. 161:140, 1965 4. Kinney, J.M.: Calories: nitrogen: disease and injury relationships. In Total Parenteral Nutrition. Acton, Mass., Publishing Sciences Group, Inc., 1974, pp. 8191 5. Wilmore, D.W., Long, J.M., Mason, A.D., Jr., Skreen, R.W., Pruitt, B.A., Jr.: Catecholamines: mediator of the hypermetabolic response to thermal injury. Ann. Surg. 186:53, 1974 6. Wilmore, D.W.: Nutrition and metabolism following thermal injury. Clin. Hast. Surg. 1:603, 1974 7. Wilmore, D.W., Orcutt, T.W., Mason, A.D., Jr., Pruitt, B.A., Jr.: Alterations in hypothalamic function following thermal injury. J. Trauma /5:697, 1975 8. Bradham, G.B.: Direct measurement of total metabolism of a burned patient. Arch. Surg. 105:410, 1972 9. Roe, C.F.: Temperature regulation and energy metabolism in surgical patients. Prog. Surg. 12:93, 1973 10. Loebl, E.C., Marvin, J.A., Heck, E.L., Curreri, P.W., Baxter, C.R.: The use of quantitative biopsy cultures in bacteriologic monitoring of burn patients. J. Surg. Res. 16:1, 1974 11. Loebl, E.C., Marvin, J.A., Heck, E.L., Curreri, P.W., Baxter, C.R.: The method of quantitative burn wound biopsy cultures and its routine use in the care of the burned patient. Am. J. Clin. Pathol. 61:20, 1974 12. Curreri, P.W., Marvin, J.A.: Advances in the clinical care of burned patients. West. J. Med. 123:275, 1975 13. Wilmore, D.W., Curreri, P.W., Spitzer, K.W., Spitzer, M.E., Pruitt, B.A., Jr.: Supernormal dietary intake in thermally injured hypermetabolic patients. Surg. Gynecol. Obstet. 132:881, 1971 14. Curreri, P.W.: A long-term supernormal caloric dietary program in extensively burned patients. In Intravenous Hyperalimentation, G.S.N. Cowan, Jr., W.L. Scheetz, editors. Philadelphia, Lea and Febiger, 1972, pp. 136-141 15. Curreri, P.W., Richmond, D., Marvin, J.A., Baxter, C.R.: Dietary requirements of patients with major burns. J. Am. Diet. Assoc. 65:415, 1974 16. Dudrick, S.J., Wilmore, D.W., Vats, H.M.: Longterm total parenteral nutrition with growth, development, and positive nitrogen balance. Surgery 64:134, 1968 17. Meng, H.C.: Fat emulsions. In Total Parenteral Nutrition. Acton, Mass., Publishing Science Group, Inc., 1974, pp. 178-179 18. Long, J.M., Wilmore, D.W., Mason, A.D., Jr., Pruitt, B.A., Jr.: Comparison of carbohydrate and fat as caloric sources. Surg. Forum 26:108, 1975 19. Newsome, T.W., Mason, A.D., Jr., Pruitt, B.A., Jr.: Weight loss following thermal injury. Ann. Surg. 178:215, 1973 20. Reckler, J.M., Bruck, H.M., Munster, A.M., Curreri, P.W., Pruitt, B.A., Jr.: Superior mesenteric artery
P.W. Curreri: Nutritional Support of Burn Patients
syndrome as a consequence of burn injury. J. Trauma 12:979, 1972 21. Alexander, J.W.: Emerging concepts in the control of surgical infections. Surgery 75:934, 1974 22. Law, D.K., Dudrick, S.J., Abdau, N.I.: The effects of protein caloric malnutrition on immune competence of
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the surgical patient. Surg. Gynecol. Obstet. 139:257, 1974 23. Curreri, P.W., Hicks, J.E., Aronoff, R.J., Baxter, C.R.: Inhibition of active sodium transport in erythrocytes from burn patients. Surg. Gynecol. Obstet. 139:538, 1974.
Invited Commentary C. Francis Roe, M.D. Yale UniversitySchoolof Medicine, New Haven, Connecticut,U.S.A.
The problem of nutritional maintenance is widespread in surgical practice, and nowhere more important than in the care of severely burned patients. As Curreri points out, hypermetabolism is a major factor in such patients. The rate of energy expenditure in severely injured patients with nonthermal injuries, such as multiple long bone fractures, may be increased by up to 25% of the resting value, but severely burned patients can show a doubling of their resting rate of energy expenditure, a large increase approximately equivalent to the energy required for continuous jogging. This means that in order to keep in nutritional balance, up to 5,000 Kilocalories must be administered daily, absorbed, and converted into usable form. The very magnitude of this problem begets secondary problems. The rule-of-thumb calorie value for most of the hyperalimentation preparations, both enteral and intravenous, is 1 kcal/ml, which means that the patient has somehow to deal with a large fluid volume overload in addition to the problems of hyperosmolarity and electrolyte imbalance which are well described in Curreri's paper. How well are these calories utilized? How much nitrogen wastage continues during such hyperalimentation? What is the effect of sepsis on utilization of these exogenous calories? Although all these questions have been addressed at one time or another, satisfactory quantitative answers are needed to make nutritional support of these patients less of a haphazard undertaking. The science of burn treatment is bedecked with formulas, such as the Brooke formula, the Moore budget, and the Evans formula, to mention only a few. They have served as rough guidelines for early treatment and are still valid in situations where accurate measurements cannot be carried out. Likewise, Curreri's formula has value in estimating the broad outlines of the energy requirements of burned pa-
tients, but it must be remembered that large variations in energy requirements exist in patients who have suffered burns of similar magnitude. These variations depend on factors such as the use of occlusive dressings, the ambient temperature and humidity of the patient's environment, and the presence or absence of sepsis and fever. Thus, in institutions where such measurements can be carried out, actual measurements of energy expenditure by indirect calorimetry techniques are extremely useful as a basis for evaluating ongoing nutritional requirements. Curreri's paper admirably describes the difficulties and problems associated with attempting to provide sufficient calories to the hypermetabolic burn patient. These difficulties are substantial to say the least, ranging from problems in administering the huge caloric requirements to the impairment of wound healing and erythrocyte function resulting from inadequate nutritional support. Intravenous hyperalimentation catheters, even when inserted and maintained with all possible care, are liable to get infected, with potentially disastrous consequences. In nonburn patients, catheter sepsis is usually announced by fever, chills, and hyperglycemia associated with a diminished rate of glucose utilization. In severely burned patients, these vital indicators may be masked or mimicked by other factors directly related to the burn injury. For instance, the normal cutaneous control of body temperature by vasomotor activity and sweating is impaired in proportion to the extent and severity of the burn, with resulting poorly controlled swings in body temperature. Thus, an important indicator of catheter sepsis may be lost with a potentially lethal delay in diagnosis. The diminished ability of the depleted burn patient to handle sepsis adds to the hazards of this form of therapy. The potential benefits of intravenous hyperalimentation are so great, however, that these risks some-
