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Nutrition Strategies in Neurotrauma
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Neurotrauma
Nutrition Strategies in Neurotrauma Jill Donaldson, MSN, RN, CCRN, CS, Marcello A. Borzatta, MD, FAGS, and Debbie Matossian, RD, CNSD
Following traumatic brain injury, providing adequate nutritional support can be an unsuspected challenge. New information is perpetually being added to the understanding of neurotrauma as well as to that of nutritional requirements during critical illness. Although emphasis is placed on preventing secondary injury such as infection, pneumonia, and organ failure, adequate nutritional support is a major component in safeguarding against these complications. This article provides a review of metabolic changes that occur following head injury, a literature review of metabolic and nutritional requirements, and current strategies designed to meet nutritional requirements of patients following neurotrauma.
Metabolic Response to Neurotrauma The metabolic state following neurotrauma differs from that of a healthy individual because of the body's hypermetabolic response to the insult of injury. Hypermetabolism seems to be initiated by factors such as dead tissue, injured tissue, perfusion deficits, and invading organisms. 4 The initial metabolic re-
From the Mission Hospital Regional Medical Center, Mission Viejo, California
sponse to injury, known as the ebb or shock phase, tends to peak 48 to 72 hours postinjury and then subsides during the following 3 to 4 days. 8 The ebb phase is represented by altered vascular permeability, a decrease in body temperature, hyperglycemia, and an overall reduction in energy expenditure. Following the ebb phase, the flow phase begins and lasts from a few days to weeks depending on the degree of injury. It is a hypermetabolic, hypercatabolic state derived from release of counteregulatory hormones such as insulin, glucagon, cortisol, epinephrine, and norepinephrine. 5 Hypermetabolism generates an increase in energy expenditure, oxygen consumption (Vo 2), carbon dioxide production (Vco 2), and metabolic acid production. The body responds by using amino acids, carbohydrates, and fat for energy, resulting in a negative nitrogen balance and catabolism. 5· 44 Nutritional management must be aimed at increasing caloric intake to meet the increased metabolic rate. Patients sustaining severe head trauma have been found to experience a significant hypermetabolic, hypercatabolic state. 30· 41 Researchers have found that head-injured patients have a resting energy expenditure that is 169% greater than expected in normal, healthy individuals. 30 Head-injured patients may continue to have an increased metabolic rate in spite of paralysis, which suggests that
CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 I Number 4 I December 2000
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muscle tone alone does not account for the hypermetabolic state. 7 In contrast, significant hypometabolism is found to be present in neurosurgical patients receiving barbiturates, neuromuscular blocking agents, and braindead patients. 10• 13 In addition, significant hyperglycemia is common following head injury and is present during both the ebb and flow phases of injury. Hyperglycemia seems to occur because of an increased production of glucose relative to net utilization and resistance to insulin. 12 Hyperglycemia has been found to adversely affect outcome following neurotrauma by causing further damage to ischemic cells. 20 • 25 Practitioners must be continuously aware of each of these metabolic alterations so that they may be addressed and treated promptly.
Estimating and Predicting Energy Expenditure One of the key issues in nutritional assessment is accurately quantifying the degree of hypermetabolism. There are two basic methods for determining caloric needs: (1) indirect calorimetry and (2) a predictive equation known as the Harris-Benedict equation. The most accurate method of measuring energy expenditure in mechanically ventilated, critically ill patients, is indirect calorimetry (Fig. 1). Indirect calorimetry is the method by which energy expenditure is estimated from measurements ofVo 2 , Co 2 , and Vco 2 • The procedure is noninvasive, is performed at the bedside, and can be used to investigate numerous aspects of metabolism, heat produc-
Figure 1 Indirect calorimetry is used to calculate energy expenditure by measuring oxygen consumption and C0 2 production in 1-minute intervals until a steady state is achieved. Measures of resting energy expenditure (REE) are in kcal/24 h. A portable Sensormedics Deltatrac Metabolic Monitor (Anaheim, CA) is shown.
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tion, and energy The routine use of indirect calorimetry to guide caloric supplementation in neurotrauma patients is warranted because of the high degree of variability in the metabolic response to traumatic brain injury. 41 The Harris-Benedict equation estimates basal energy expenditure (BEE). Basal energy expenditure is an estimate of resting energy requirements and is defined as the energy required to maintain life-sustaining processes when the body is at rest and in a fasting state. It is a mathematical formula commonly used to estimate caloric requirements using weight in kilograms (w), height in centimeters (h), sex, and age in years (a) in kilocalories per 24 hours Equation 1. 16 Unfortunately, it predicts the average energy requirement for a normal, healthy individual and not the requirements of the critically ill. An injury correction factor is used in conjunction with the Harris-Benedict equation to account for the hypermetabolic state. It is a numerical value that represents the average increment in metabolic expenditure observed in specific populations of patientsr Researchers recommend that BEE X 1.4 be used for nonparalyzed neurotrauma patients, whereas BEE X 1.0 be used for paralyzed neurotrauma patients. 3 Despite this recommendation, these injury correction factors may be useful only during an initial assessment. Caloric requirements must be reevaluated and adjusted frequently.
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of the gastrointestinal (GI) tract. The enteral route should always be considered first if GI function is adequate, yet the argument in favor of the parenteral route remains strong.
Parenteral Nutrition The parenteral route is an effective method of providing necessary calories, fluids, and electrolytes following neurotrauma. Historically it has been preferred in neurotrauma because of the high incidence of gastric intolerance. The parenteral route allows a faster achievement of caloric goals when compared with the enteral route, and researchers believe that early parenteral nutrition is associated with improved patient outcomes following neurotrauma and enhanced immunologic function. 33 36. The parenteral route is often perceived as a risk because it requires the administration of large volumes of fluids in traditionally fluid-restricted patients. However, studies comparing brain-injured patients with severe injuries receiving parenteral and enteral nutrition show no difference in the rate of increased intracranial pressure .15 If the parenteral route is selected initially, consideration should still be given to converting to the enteral route as soon as possible. Although complications with attaining nutritional goals exist with the use of enteral nutrition, research in support of the enteral (gastric or jejuna!) route outweighs that of the parenteral route when it is relied on as a sole source of nutritional support.
Nutritional Support There are three options for the delivery of nutritional support, parenteral (intravenous), enteral-gastric (stomach), and enteral-jejunal (small intestine), in the critically ill. The method of delivery depends on the function
Equation 1
THE HARRIS-BENEDICT
EQUATION TO ESTIMATE BASAL ENERGY EXPENDITURE (BEE) BEE male= 66 + (13.7 >< w) + (5 x h) - (6.8 x a) BEE female = 655 + (9 6 x w) + (1.7 x h) - (4.7 x a) w = weight in kilograms; h = height in centimeters; a = age in years
Enteral Nutrition The enteral-gastric route is feasible only when gastric emptying is adequate, with or without the use of a prokinetic agent such as metoclopramide. The decision to select the enteral route involves weighing the risk of gastric intolerance versus delaying achievement of caloric goals. Gastric tolerance is inversely related to the severity of increased intracranial pressure from brain injury and has been found to be delayed or abnormal in most neurotrauma patients during the first 2 weeks postinjury. 3132 Additionally, feeding tube displacement, surgery, presence of blue food coloring in oropharynx, diarrhea, and abdominal distention can result in cessation of enteral tube feeding and may quickly result in inadequate caloric intaken· 39 · 40
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The jejunal route is preferred over gastric feedings because of the idea that "ileus" is localized in the stomach. Feedings can be administered directly into the jejunum, bypassing the stomach, and absorption of nutrients can occur without symptoms of intolerance. Data strongly support the use of the jejunal route based on improved gastric tolerance, lower theoretic risk of infection, lower cost, and the elimination of hyperglycemia associated with parenteral nutrition. 3 Some studies have attempted to evaluate the effect of gastric and jejunal feedings on patient outcome. Jejunal-fed subjects have significantly lower infection rates and intensive care unit stay, receive significantly higher proportions of their daily caloric intake, and have significantly greater increases in serum prealbumin and lower rates of pneumonia than patients fed by continuous gastric feeding. 14 , 29 The success of the jejuna! route for administering feedings following neurotrauma has drawn attention to achieving small bowel (jejuna!) access. Small-bore feeding tubes placed past the pyloris and ligament of Treitz, into the jejunum, allow for the delivery of enteral nutrition in patients with gastroparesis. It is commonly assumed that neuromuscular blocking agents, sedatives, and analgesics used in the treatment of neurotrauma interfere with gastric function and feeding tolerance. Postpyloric jejuna! feedings, however, are well tolerated, even during the administration of pentobarbital. 24 Spontaneous jejunal (postpyloric) feeding tube placement has recently become popular with the use of a prokinetic agent that eliminates radiologic or endoscopic intervention. Lord identified the following bedside protocol to achieve jejuna! placement: 10 mg metoclopramide intravenously, wait 10 minutes, and insert all but the last 10 inches of a 36-inch feeding tube. 22 This procedure resulted in 88% postpyloric placement within 4 hours using an 8 F unweighted small-bore feeding tube in intensive care unit patients. These findings have not been duplicated in neurotrauma patients so endoscopic or fluoroscopic guidance may be necessary if normal motility fails to migrate the feeding tube past the pyloris.
Enteral Formula Selection Because protein requirements are accentuated after neurotrauma, the protein compo-
nent is the most significant factor to consider.11 It has been suggested that initial metabolic requirements should be met while providing 15% of calories as protein as found in traditional formulas. 3 At Mission Hospital Regional Medical Center, the Metabolic Support Team advocates starting a high-protein formula such as lsosource 1.5 (Novaritis, Minneapolis, MN), a concentrated (1.5 calories per mL) formula providing 18% of calories from protein. The smaller volume of concentrated formulas is found to be better tolerated. If the patient is determined to be extremely catabolic, lsosource VHN (Novartis), providing 25% of calories as protein, is initiated. Protein content is also categorized by digestibility. Enteral formulas are available with intact protein, partially hydrolyzed protein, peptide-based protein, and crystalline amino acids, for varying degrees of digestive capacities (Table 1). Studies examining the effect of peptide-based enteral formulas indicate that they may improve visceral protein levels, such as prealbumin, and a lower incidence of diarrhea.28 Many institutions advocate the use of peptide-based formulas when feeding into the small bowel, but the high cost of these formulas and lack of documented effect on patient outcome should be considered. Ultimately, formula selection should be based on individual needs and absorptive capacity of the patient.
Targeting Caloric Requirements An accurate estimation of metabolic requirements is crucial to avoid complications of underfeeding and overfeeding. If a patient is fed insufficiently, starvation can magnify the depletion of body tissues and contribute to organ function impairment. Researchers have identified an association between multipleorgan failure and a large caloric deficit. 1Major organs deplete their structural proteins to meet the body's energy requirements to the point where the organ itself becomes inefficient and organ failure ensues. 15 In general, underfeeding delays wound healing and decreases resistance to infection. 18 The small intestine, with its large quantity of lymphoid tissue, seems to be largely responsible for immune function. It is believed to have a significant role as a protective organ by guarding against translocation of bacteria. Research in-
NUTRITIQ1\j STRATEGIES IN i\IEUROTRAUMA
PROTEIN CONTENTOF ENTERA.L FORMULAS
Type of Protein
Digestion Required
Intact protein (i11 complete and original form as found in whole foods)
Yes
Partially hydrolyzed protein
Yes
Peptide-based proteins (dipeptides and tripeptides) are proteins that have been enzymatically hydrolyzed into smaller peptide fragments
No
Crystalline amino acids
No
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BY DIGESTiBIUTY
Special Characteristics
0
For patients with normal digestive capacity and normal pancreatic enzyme activity Promotes greater stimulation of gut hormone release than amino acid formulas For patients with reduced small bowel absorptive capacity Promotes greater stimulation of gut hormone release than amino acids May be used when feeding into the small bowel May improve visceral protein levels, such as prealbumin Absorbed directly into the bloodstream via passive diffusion across intestinal mucosa (does not require sodium pump) May increase absorption of sodium and water, resulting in a lower incidence of diarrhea Requires no further digestion in the gastrointestinal tract. Requires sodium pump for active transport of nutrients across intestinal mucosa For patients with reduced small bowel absorptive capacity Adds considerably to hyperosmolality
Data from ldeno K: Enteral nutrition. In Gottschlich M, Materase L Nutritional support dietetics core curriculum, ed 2. Silver Spring, MD, Aspen, 1993, p 75; and MacBurney M, Russel C, Young LS: Formulas. In Rambeau JL, Caldwell MD Clinical Nutrition Enteral and Tube Feeding, ed 2. Philadelphia, WB Saunders, 1990.
clicates that gut function and integrity begin to deteriorate when the body is in a state of starvation. 21 For example, animal studies have determined that within 24 to 72 hours following a burn injury, the intestine becomes edematous and begins to atrophy and bacterial translocation occurs. 3°For obvious reasons, researchers are unable to duplicate this type of animal in vivo research in humans, and therefore the concept continues to be evaluated. On the other hand, overfeeding is harmful as well. Supplying too many calories can cause hepatic dysfunction, hyperglycemia, elevated levels of blood urea nitrogen (BUN), cholesterol, and triglycerides. Large amounts of glucose calories given to ventilatordependent patients can lead to an increase in C0 2 , which may impede ventilator weaning. 2 9 Planning and targeting an accurate estimation of caloric requirements is imperative for optimizing the patient's metabolic requirements.
Timing of Nutritional Support Nutritional support should be instituted within 24 hours of admission, and caloric
goals should be met within 48 hours. Because of the incidence of gastric intolerance following head injury, establishing nutritional goals quickly while simultaneously treating increased intracranial pressure can be difficult. The route of administration and formula selection should be based on individual patient need, yet a consistent approach to establishing and meeting nutritional requirements is helpful. The body can \Nithstand a short period of starvation, but we now know that recovery may be improved with the early introduction of nutritional support. It seems that delayed enteral feeding (more than 5 clays) fails to provide a reduction in complications, but early enteral feeding (less than 48 hours) is important to maintain resistance to infection. 19 Early enteral feeding has been found to be associated with improved blood flow to the intestine with preservation of gut mucosa! integrity and reduced hypermetabolic response (when compared with the parenteral nutrition). There is an abundance of evidence supporting the idea that early enteral nutrition improves recovery, decreases complications
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and infections, and improves wound healing.38 A recent study evaluated the effect of early enteral nutrition in head-injured patients when targeted caloric requirements were met on day 1. 42 There were fewer overall complications and a reduction in the postinjury inflammatory response when compared with control patients (target caloric requirements met after day 1). We may infer that patients fed enterally have better outcomes because enteral nutrition maintains the gut, an immunologically significant organ.
Administration of Nutritional Support Versus Fluid Volume Prompted by the development of "Guidelines for the Management of Severe Head Injury" in 1995 (authored by members of the American Association of Neurological Surgeons [AANS]/CNS Joint Section on Neurotrauma and Critical Care and supported by the Brain Trauma and AANS), practitioners have witnessed a significant change in practice that has had a considerable impact on the management of nutritional support. 3 The maintenance of normovolemia, which the AANS guidelines support, has eased the predicament of providing adequate calories to headinjured patients in the face of fluid restriction. Now, nutritional support is not secondary to maintaining serum osmolality and intracranial pressure. No longer must volume-restricted head-injured patients wait for days and then receive only a portion of their daily caloric requirements because of increased intracranial pressure. This change in practice has had a significant impact on the quality of nutritional support provided to head-injured patients and demands that practitioners reevaluate old practices. Maintenance of adequate nutritional support by means of preserving normovolemia alone could quite possibly be a major influence on patient outcomes following major head injury.
Monitoring Nutritional Support Nitrogen balance can be used to estimate nutritional needs and evaluate the adequacy of protein intake. A positive nitrogen balance is the goal (nitrogen intake exceeding loss), even though it is often difficult or impossible to obtain during the catabolic state. In addi-
tion, urine urea nitrogen (UUN) collections (normal range, 12 to 20 g per 24 hours) are not precise for determining nitrogen losses during the catabolic state but are useful for monitoring the extent of catabolism. A catabolic state may be identified by a negative nitrogen balance that occurs despite adequate dietary protein intake (1.5 g/kg per day). Nitrogen balance is determined by calculating the amount of nitrogen intake from the diet minus nitrogen excretion (Equation 2). Prealbumin, with a half-life of 2 days, is a biologic nutritional marker indicative of a patient's nutritional and nitrogen status. Its normal range is 10.6 to 42.4 mg/dL. Although the accuracy of prealbumin measurements is also affected by the catabolic state, it is commonly used along with indirect calorimetry and UUN to assist in guiding nutritional support supplementation. _J_I\_ useful guideline, as reported by Roberts, is to monitor prealbumin levels after 3 to 5 days on the goal rate for a given formula and weekly thereafter once it appears that metabolic needs are being met. 34 Serum mineral levels are also affected following injury, in particular, zinc, iron, and copper. Increased urinary zinc excretion has been reported in head-injured patients, which lasts up to 3 weeks. 26 · 44 Several small studies have examined the effect of zinc supplementation in head-injured patients during the immediate postinjury period. Zinc supplementation seems to be associated with improved neurologic outcome and enhanced prealbu-
Equation 2 EQUATION TO DETERMINE NITROGEN BALANCE (PROTEIN BALANCE) Protein is metabolized for energy during catabolism and must be replaced with exogenous protein to avoid protein malnutrition. The goal is to offset a loss of protein mass by infusing protein or amino acids enterally or parenterally. Values of +4 to +6 indicate an anabolic state; + 1 to -1, a homeostatic state; and less than -2, a catabolic state.
Prote~n2 ~take - (UUN excreted + 4') '4 accounts for other nitrogen losses (2 g stool g skin). UUN = urine urea nitrogen
+2
NUTRITION STRATEGIES l1N NEUROTRAUMA
min levels. 16 Zinc may be considered when scrum zinc concentrations are low.
Guidemines for Enteram INutrH:fonal Support in the Neurotrauma Patient Recent literature has outlined early enteral nutrition protocols in head-injured patients, 34 • 42 but there is little other information available to guide a standard of practice. The initiation of nutritional support following severe head injury should begin within the first 24 hours following admission. Gastric feeding is preferred because it is less expensive, and formulas can be delivered while taking advantage of the normal process of digestion and absorption. The jejuna! route should be used when gastroparesis persists, and it is often necessary in ncurotrauma during the first 4 to 5 clays postinjrny. A concentrated, full-strength formula may be attempted at a rate of 20 to 30 mL/h to evaluate tolerance. If the gastric route is successful, with or without the use of a prokinetic agent, gastric residuals should be monitored every 4 hours. If the enteral-jejunal route is achieved evidence of abdominal distention should b~ assessed. If continued evidence of gastric intolerance occurs with higher feeding rates (gastric or jejuna!), the addition of parenteral nutrition may be warranted to meet targeted caloric goals. Initially, calories should be limited to BEE X 1.0 for mechanically ventilated, pharmacologically paralyzed head-injured patients, and BEE X 1.4 for all others. Indirect calorimetry should be performed on eve1y mechanically ventilated patient by clay 5 if mechanical ventilation is anticipated to exceed 9 clays. Routine monitoring should include nutrient intake, signs of intolerance to therapy, weight changes, and biologic, hematologic, and other pertinent diagnostic data. A guideline is provided based on literature review and current practice at Mission Hospital Regional Medical Center (Appendix
CASE HISTORY A 27-year-olcl female patient was transferred to the surgical intensive care unit following a craniotomy for a large left pari-
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etal subdural hematoma that she sustained after falling from a window. Her intracranial pressure remained elevated postoperatively and required management with continuous propofol drip, analgesics, and paralytics. A nonweighted, small-bore feeding tube was placed on postoperative clay 1, and postpyloric placement was achieved within 12 hours following administration of a prokinetic agent, metoclopramide. She was started on a concentrated enteral formula at 20 mL/h (Isosource 1.5), which provided 720 calories per day. Within the following 12 hours, her goal rate was increased to 40 mL/h, providing her 102% of her estimated caloric requirements. Her initial caloric goal was set to approximate the I3EE of 1449 (based on a height of 5' 6" and weight of 140 pounds) as estimated by the Harris-Benedict equation. Fat calories provided by propofol (a lipidbased drug providing 1.1 kcal/mL) were included in the calorie count. Serum triglyceride concentration was performed before propofol administration and then followed eve1y other clay to monitor for hypertriglycericlemia. An indirect calorimetry measurement was performed on day 3, which indicated a need for 2029 kcal per 24 hours 140% above the BEE. Isosource 1.5 was i~creased accordingly (full strength) at 50 mL/h in combination with 384 mL per 24 hours of propofol, providing 2222 kcal and 13 g nitrogen, about 109% of the measured energy expenditure. Upon admission, prealbumin (13 mg/dL) was borderline low and 24-hour UUN was within normal limits (12 g per 24 hours). Serial laboratory tests indicated an increase in prealbumin on day 4, suggesting adequate nutritional clelive1y. The 24-hour UUN, however, was 15.6, resulting in a negative nitrogen balance. Because propofol was discontinued on clay 5, this allowed the dietitian to provide more calories in the form of protein, and an isotonic, highprotein formula was ordered (Isosource VHN at 85 mL/h) providing 2040 kcal and 20.2 g nitrogen, approximately 100% of both caloric and protein needs. Neurosurgical therapy to control intracranial pressure was weaned on clays 10 through 12. The patient was able to open
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her eyes, move all extremities purposefully, and follow simple commands. Indirect calorimetry was performed again, and it indicated an increase in estimated needs (2202 kcal per 24 hours), 152% of BEE. Ventilator support was discontinued on day 13, and a swallowing evaluation was performed on day 15. A dysphagic diet consisting of thickened liquids was ordered, and the patient was able to consume about
50% (1120 kcal) of her diet. Night-time enteral feedings were ordered (6 PM to 6 AM) to supplement her diet, and she was transferred from the intensive care unit on day 16. Daily calorie counts were maintained, and the patient was able to consume 75% of a soft diet by day 20 (80% of estimated caloric requirements). Enteral feedings were discontinued, and the patient continued to have steady neurologic improvement.
A basic understanding ofmetabolicalterationsthat occur following neurotrauma is essential for addressing nutritional requirements. Interventions must be rese.arch based and must focus on the support ofmetabolicalterations, miniillizing the effect of catabolism and optimizing caloric delivery to meet metabolic demand. The goal of accuracy in the delivery of nutritional support is to ensure a reduction inpatient morbidity. Nutritional support requires an ongoing, daily assessment of caloric goals, protein requirements, patient responses, and assessment of nutritional laboratory values. Using this strategy, neurotrauma patients will have the greatest opportunity for a positive outcome.
ACKNOWLEDGMENTS The authors wish to express their thanks and appreciation to the administrative, medical, and nursing staff of Mission Hospital Regional Medical Center, Mission Viejo, California. Their support of the Metabolic Support Team has made it a continuing success for over a decade.
REFERENCES 1. Bartlett RH, Dechert RE, Mault JR: Measurement of metabolism in multiple organ failure. Surgery 92:771, 1982 2. Benotti PN, Bistran B: Metabolic and nutritional aspects of weaning from mechanical ventilation. Crit Care Med 17:181, 1989 3. Bullock R, Chestnut RM, Clifton G, et al: Guidelines for the Management of Severe Head Injury. New York, Brain Trauma Foundation and American Association of Neurological Surgeons, 1995, pp 14-1-14-15 4. Cerra FB: Hypermetabolism, organ failure, and metabolic support. Surgery 101:1, 1987 5. Chiolero R, Schutz Y, Lemerch T, et al: Hormonal and metabolic changes following head injury or noncranial injury. J Parenter Enteral Nutr 13:5, 1989 6. Clifton G, Robertson C, Choi S, et al: Assessment of nutritional require1nents of head-injured patients. J Neurosurg 64:895, 1986 7. Clifton G, Roberton C, Grossman R, et al: The metabolic response to severe head injury. J Neurosurg 60:687, 1984
8. Cuthbertson DP: Alterations in metabolism following injury: Part 1. Injury 11:175, 1980 9. Dark D, Pingleton S, Kerby G: Hypercapnia during weaning: A complication of nutritional support. Chest 88:141, 1985 10. Dempsey DT, Guenter P, Mullen JL, et al: Energy expenditure in acute trauma to the head with and without barbiturate therapy. Surgery Gynecology and Obstetrics 160:128, 1985 11. Dickerson RN, Guenter PA, Gennarelli TA, et al: Increased contribution of protein oxidation to energy expenditure in head-injured patients. J Am Coll Nutr 9:86, 1990 12. Flakoll P, Wentzel L, Hyman S: Protein and glucose metabolism during isolated closed-head injury. Am J Physiol 269:636, 1995 13. Gadisseux P, Ward J, Young H: Nutrition and the neurosurgical patient. J Neurosurg 60:219, 1984 14. Graham TW, Zadrozny DB, Harrington T: The benefits of early jejuna! hyperalimentation in the heaclinjurecl patient. Neurosurgery 25:729, 1989 15. Grant JP: Clinical impact of protein malnutrition on organ mass and function. In Blackbum GL, Grant JP, Young VR (eels): Amino Acids, Metabolism and Medical Application. Boston, MA, 1990, pp 347-358 16. Harris JA, Benedict FG: A biometric study of basal metabolism in man (pub no 279). Washington DC, Carnegie Institute of Washington, 1919 17. Ideno K: Entcral nutrition. In Gottschlich I\1, ~/Iatcre:-:;e L: Nutritional support dietetics core curriculum, ed 2. Silver Spring, MD, Aspen, 1993, p 75 18. Keenan RA, Molclawer LL, Yang RD, et al: An altered response by peripheral leukocytes to synthesize or
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release leukocyte endogenous mediator in critically ill, protein-1rn1lnourished patients . .J Lah Clin Med 100:844, 1982 19. Kuclsk KA, Minard G: Enteral nutrition. In Zaloga GP (eel): Nutrition in Critical Care. Mosby, St Louis, MO, 1994, p 334 20. Lam AM, Winn R, Cullen BF, et al: Hyperglycemia and neurological outcome in patients with head injury. .J Neurosurg 75:545, 1991 21. Lord Ll'vl, Sax HC: The role of the gut in critical illness. AACN Clinical Issues in Critical Care Nursing 5:450, 1994 22. Lord Ll'vl, Weiser-Maimone A, Pulhamus M, et al: Comparison of weighted vs unweighted enteral feeding tubes for efficacy of trans pyloric intubation. JPEN J Parenter Enteral Nutr 17:271, 1993 23. Madlurney M, Russel C, Young LS: Formulas. In Rombeau JL, Caldwell MD: Clinical Nutrition: Enteral and Tube Feeding, eel 2. Philadelphia, WB Saunders, 1990 24. Magnuson B. Hatton J, Williams S, et al: Tolerance ;:incl efficacy of enteral nutrition for neurosurgical patients in pentobarbital coma. Nutrition in Clinical Practice 14:131, 1999 25. Marie C, Bratlet J: Blood glucose level and morphological brain damage following cerebral ischemia. Cerebrovascular and Brain Metabolism Reviews 3:29, 1991 26. McClain C, Twyman D, Ott L, et al: Serum and urine zinc response in head-injured patients. J Neurosurg 64:224, 1986 27. McClave SA, Sexton LK, Spain DA, et al: Enteral tube feeding in the intensive care unit: Factors impeding adequate delivery. Crit Care Med 27: 1252, 1999 28. Meredith JW, Ditesheim JA, Zaloga GP: Visceral protein levels in trauma patients are greater with peptide diet than with intact protein diet. J Trauma 30:825, 1990 29. Montecalvo J'vIA, Steger KA, Farber HW, et al: Nutritional outcome and pneumonia in critical care patients randomized to gastric versus jejuna! tube feedings: The Critical Care Research Team. Crit Care Med 20:1377, 1992 30. Moore R, Najarian MP, Konvolinka CW: Measured energy expenditure in severe head trauma. J Trauma 29: 1633, 1989 31. NortonJA, Ott LH, McClain C: Intolerance to enteral feeding in the br;:iin-injured patient. J Neurosurg 68:62, 1988 32. Ott L, Young B, Phillips R, et al: Altered gastric emptying in the head-injured patient: Relationship to feeding intolerance. J Neurosurg 74:738, 1991
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33. Rapp RP. Young B, Twyman D, et al: The favorable effect of early parenteral feeding on survival in headinjured patients. J Neurosurg 58:906, 1983 34. Roberts PR: Nutrition in the head-injured patient. New Horizons 3:506, 1995 35. Saito H, Trocki 0, Alexander JW, et al: The effect of route of nutrient administration on the nutritional state, catabolic hormone secretion, and gut mucosa! integrity after burn injury. JPEN J Parenter Enteral Nutr 11:1, 1987 36. Sacks GS, Brown OR, Teague D: Early enteral nutrition support modifies immune function in patients sustaining he;:id injury. JPEN J Parenter Enteral Nutr 19:387, 1995 37. Schlichtig R, Ayres AJ'vl: Nutritional Support of the Critically III. Chicago, IL, Year Book Publishing, 1988 38. Schroeder D, Gillanders L, Mahr K, et al: Effects of immediate postoperative enteral nutrition on body composition, muscle function, and wound healing. JPEN J Parenter Enteral Nutr 15:376, 1991 39. Spain DA, McClave SA, Sexton LK, et al: Infusion protocol improves delivery of enteral tube feeding in the critical care unit. JPEN J Parenter Enteral N utr 23:288, 1999 40. Stechmiller J, Treloar DM, Derrico D, et al: Interruption of enteral feedings in head injured patients. J Neurosci Nurs 26:224, 1994 41. Sunderland P, Heilbrun M, et al: Estimating energy expenditure in traumatic brain injury: Comparison of indirect calorimetry with predictive formulas. Neurosurgery 31:246, 1992 42. Taylor SJ, Fettes SB, Jewkes C, et al: Prospective, randomized, controlled trial to determine the effect of early enhanced enteral nutrition on clinical outcome in mechanically ventilated patients suffering head injury. Crit Care Med 27:2525, 1999 43. Varella I: Head and spinal cord injury. In Hennessy K, Orr M: Nutrition Support Nursing Core Curriculum, eel 3. Silver Spring, MD, Aspen. 1996, pp 13-7, 13-8 44. Young B, Ott L, Beard D, et al: The acute-phase response of the brain-injured patient. J Neurosurg 69 375, 1988 45. Young B, Ott L, Haack D: The effect of total parenteral nutrition upon intracranial pressure in severe head injury. J Neurosurg 67:76, 1987 46. Young ll, Ott L, Kasarskis E, et al: Zinc supplementation is associated with improved neurologic recovery rate and visceral protein levels of patients with severe closed head injury. J Neurotrauma 13:25, 1996 47. Young B, Ott L, Twyman D: The effect of nutritional support on outcome from severe head injury. J Neurosurg 67:668, 1987 Address reprint requests to Jill Donaldson, MSN, RN, CCRN, CS Vascular Institute and Stroke Center Mission Hospital Regional Medical Center 27700 Medical Center Road Mission Viejo, CA 92691
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Appendix 1. Guidelines for Enteral Nutritional Support in the Neurotrauma Patient The goal of nutritional support in the neurosurgical patient is to begin a feeding regimen within the first 24 hours following admission with the goal of achieving the targeted nutritional goal within 48 hours. A. The preference is to begin a trial of gastric feeding and to determine gastric intolerance (i.e., gastric residual of more than 150 ml) before attempting postpyloric placement of feeding tubes. However, if a small-bore feeding tube can be successfully placed at the bedside with the aid of a prokinetic agent, this initial attempt at postpyloric placement is recommended. The small-bore feeding tube should be longer than 36 inches to maintain position in the small bowel. If unsuccessful, postpyloric placement may require endoscopic or fluoroscopic guidance. Small-bore feeding tubes should be longer than 36 inches to maintain position in the small bowel. B. Maintain the head of bed at 30° or more. C. Administer prokinetic agent such as metoclopramide every 8 hours. D. A concentrated, full-strength formula may be attempted at a rate of 20 to 30 ml/h. E. If feeding into the stomach, gastric residuals must be monitored at least every 4 hours, and the rate may be increased every 4 hours up to the target goal unless gastric residuals exceed 150 ml. If gastric residual is greater than 150 ml, feeding should be held and residual should be checked in 2 hours. F. If feeding into the small bowel, obtain residuals every 8 hours (high residuals may indicate tube tip migration back into the stomach or a distal obstruction). An abdominal assessment should be performed every 8 hours. Inspect for distention and palpate for firmness. Abdominal girth may be monitored by marking the patient's skin and measuring the distance (tip to tip) between the iliac crests. Parenteral nutrition may be indicated if enteral feedings are unsuccessful.
G. If intolerance occurs (with gastric or jejuna! feeding), decrease feeding rate to 30 ml/h for 24 hours and advance as described in E. H. If long-term nutritional support is needed or anticipated to be longer than 6 weeks, alternative modes of delivery should be accessed, such as percutaneous endoscopic gastrostomy (PEG), percutaneous endoscopic jejunostomy (PEJ), jejunostomy tube CJ-tube), or indwelling catheter (for parenteral route). I. Initial calories should be limited to BEE X 1.0 for mechanically ventilated, pharmacologically paralyzed head-injured patients, and BEE X 1.4 for all others. Indirect calorimetry should be performed on every mechanically ventilated patient by day 5 if mechanical ventilation is anticipated to exceed 9 days. Routine monitoring will include nutrient intake, signs of intolerance to therapy, weight changes, and biologic, hematologic, and other pertinent diagnostic data. ]. A comprehensive nutritional laboratory panel, including comprehensive metabolic panel (Chem 20) and 24-hour UUN, prealbumin, and magnesium levels should be obtained after 3 to 5 days on the goal rate, and weekly thereafter if the nutritional laboratory panel is within acceptable limits. (UUN and prealbumin testing are not indicated for patients with renal failure.) K. Consider indirect calorimetry at days 3 to 5, and consider it weekly thereafter, especially if laboratory values or clinical condition is not consistent with initial assessment of caloric needs. L. If prealbumin is less than 10 mg/ dl, an adjustment in caloric goal or change to high nitrogen formula or both may be indicated. M. Insulin administration is indicated \vhen blood levels are elevated above 200 mg/ dl. N. If serum zinc is below normal (60 to 130 µ,g/ml), extra zinc may be adminis-
NUTRITION STRATEGIES IN NEUROTRAUivlA
tered. Zinc 220 mg oral sules, may be provided as a plemcnt. The capsules may be u1.,cu.Lu and administered through a feeding tube. If parenteral nutrition is indicated, 6 to 10 mg of elemental zinc may be added to the intravenous solutions daily. Zinc is also available in trace element combinations with chromium, copper, and manganese. 0. For transitional feeding following extubation, long-term mechanically venti-
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ideally should receive a evaluation before an appropriate diet order is prepared. P. Before discontinuation of nutritional support, the dietitian, nurse, or physician shall verify adequate oral intake. Discontinue when patient is able to resume adequate oral intake (more than sm11 of meals and supplements or more than two thirds of caloric goal) and patient is demonstrating stable nutritional parameters. ,,"""u"'·'
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Neurotrauma
Nutrition Strategies in Neurotrauma Jill Donaldson, MSN, RN, CCRN, CS, Marcello A. Borzatta, MD, FAGS, and Debbie Matossian, RD, CNSD
Following traumatic brain injury, providing adequate nutritional support can be an unsuspected challenge. New information is perpetually being added to the understanding of neurotrauma as well as to that of nutritional requirements during critical illness. Although emphasis is placed on preventing secondary injury such as infection, pneumonia, and organ failure, adequate nutritional support is a major component in safeguarding against these complications. This article provides a review of metabolic changes that occur following head injury, a literature review of metabolic and nutritional requirements, and current strategies designed to meet nutritional requirements of patients following neurotrauma.
Metabolic Response to Neurotrauma The metabolic state following neurotrauma differs from that of a healthy individual because of the body's hypermetabolic response to the insult of injury. Hypermetabolism seems to be initiated by factors such as dead tissue, injured tissue, perfusion deficits, and invading organisms. 4 The initial metabolic re-
From the Mission Hospital Regional Medical Center, Mission Viejo, California
sponse to injury, known as the ebb or shock phase, tends to peak 48 to 72 hours postinjury and then subsides during the following 3 to 4 days. 8 The ebb phase is represented by altered vascular permeability, a decrease in body temperature, hyperglycemia, and an overall reduction in energy expenditure. Following the ebb phase, the flow phase begins and lasts from a few days to weeks depending on the degree of injury. It is a hypermetabolic, hypercatabolic state derived from release of counteregulatory hormones such as insulin, glucagon, cortisol, epinephrine, and norepinephrine. 5 Hypermetabolism generates an increase in energy expenditure, oxygen consumption (Vo 2), carbon dioxide production (Vco 2), and metabolic acid production. The body responds by using amino acids, carbohydrates, and fat for energy, resulting in a negative nitrogen balance and catabolism. 5· 44 Nutritional management must be aimed at increasing caloric intake to meet the increased metabolic rate. Patients sustaining severe head trauma have been found to experience a significant hypermetabolic, hypercatabolic state. 30· 41 Researchers have found that head-injured patients have a resting energy expenditure that is 169% greater than expected in normal, healthy individuals. 30 Head-injured patients may continue to have an increased metabolic rate in spite of paralysis, which suggests that
CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 I Number 4 I December 2000
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muscle tone alone does not account for the hypermetabolic state. 7 In contrast, significant hypometabolism is found to be present in neurosurgical patients receiving barbiturates, neuromuscular blocking agents, and braindead patients. 10• 13 In addition, significant hyperglycemia is common following head injury and is present during both the ebb and flow phases of injury. Hyperglycemia seems to occur because of an increased production of glucose relative to net utilization and resistance to insulin. 12 Hyperglycemia has been found to adversely affect outcome following neurotrauma by causing further damage to ischemic cells. 20 • 25 Practitioners must be continuously aware of each of these metabolic alterations so that they may be addressed and treated promptly.
Estimating and Predicting Energy Expenditure One of the key issues in nutritional assessment is accurately quantifying the degree of hypermetabolism. There are two basic methods for determining caloric needs: (1) indirect calorimetry and (2) a predictive equation known as the Harris-Benedict equation. The most accurate method of measuring energy expenditure in mechanically ventilated, critically ill patients, is indirect calorimetry (Fig. 1). Indirect calorimetry is the method by which energy expenditure is estimated from measurements ofVo 2 , Co 2 , and Vco 2 • The procedure is noninvasive, is performed at the bedside, and can be used to investigate numerous aspects of metabolism, heat produc-
Figure 1 Indirect calorimetry is used to calculate energy expenditure by measuring oxygen consumption and C0 2 production in 1-minute intervals until a steady state is achieved. Measures of resting energy expenditure (REE) are in kcal/24 h. A portable Sensormedics Deltatrac Metabolic Monitor (Anaheim, CA) is shown.
NUTRITION STRATEGIES IN NEUROTRAUMA
tion, and energy The routine use of indirect calorimetry to guide caloric supplementation in neurotrauma patients is warranted because of the high degree of variability in the metabolic response to traumatic brain injury. 41 The Harris-Benedict equation estimates basal energy expenditure (BEE). Basal energy expenditure is an estimate of resting energy requirements and is defined as the energy required to maintain life-sustaining processes when the body is at rest and in a fasting state. It is a mathematical formula commonly used to estimate caloric requirements using weight in kilograms (w), height in centimeters (h), sex, and age in years (a) in kilocalories per 24 hours Equation 1. 16 Unfortunately, it predicts the average energy requirement for a normal, healthy individual and not the requirements of the critically ill. An injury correction factor is used in conjunction with the Harris-Benedict equation to account for the hypermetabolic state. It is a numerical value that represents the average increment in metabolic expenditure observed in specific populations of patientsr Researchers recommend that BEE X 1.4 be used for nonparalyzed neurotrauma patients, whereas BEE X 1.0 be used for paralyzed neurotrauma patients. 3 Despite this recommendation, these injury correction factors may be useful only during an initial assessment. Caloric requirements must be reevaluated and adjusted frequently.
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of the gastrointestinal (GI) tract. The enteral route should always be considered first if GI function is adequate, yet the argument in favor of the parenteral route remains strong.
Parenteral Nutrition The parenteral route is an effective method of providing necessary calories, fluids, and electrolytes following neurotrauma. Historically it has been preferred in neurotrauma because of the high incidence of gastric intolerance. The parenteral route allows a faster achievement of caloric goals when compared with the enteral route, and researchers believe that early parenteral nutrition is associated with improved patient outcomes following neurotrauma and enhanced immunologic function. 33 36. The parenteral route is often perceived as a risk because it requires the administration of large volumes of fluids in traditionally fluid-restricted patients. However, studies comparing brain-injured patients with severe injuries receiving parenteral and enteral nutrition show no difference in the rate of increased intracranial pressure .15 If the parenteral route is selected initially, consideration should still be given to converting to the enteral route as soon as possible. Although complications with attaining nutritional goals exist with the use of enteral nutrition, research in support of the enteral (gastric or jejuna!) route outweighs that of the parenteral route when it is relied on as a sole source of nutritional support.
Nutritional Support There are three options for the delivery of nutritional support, parenteral (intravenous), enteral-gastric (stomach), and enteral-jejunal (small intestine), in the critically ill. The method of delivery depends on the function
Equation 1
THE HARRIS-BENEDICT
EQUATION TO ESTIMATE BASAL ENERGY EXPENDITURE (BEE) BEE male= 66 + (13.7 >< w) + (5 x h) - (6.8 x a) BEE female = 655 + (9 6 x w) + (1.7 x h) - (4.7 x a) w = weight in kilograms; h = height in centimeters; a = age in years
Enteral Nutrition The enteral-gastric route is feasible only when gastric emptying is adequate, with or without the use of a prokinetic agent such as metoclopramide. The decision to select the enteral route involves weighing the risk of gastric intolerance versus delaying achievement of caloric goals. Gastric tolerance is inversely related to the severity of increased intracranial pressure from brain injury and has been found to be delayed or abnormal in most neurotrauma patients during the first 2 weeks postinjury. 3132 Additionally, feeding tube displacement, surgery, presence of blue food coloring in oropharynx, diarrhea, and abdominal distention can result in cessation of enteral tube feeding and may quickly result in inadequate caloric intaken· 39 · 40
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The jejunal route is preferred over gastric feedings because of the idea that "ileus" is localized in the stomach. Feedings can be administered directly into the jejunum, bypassing the stomach, and absorption of nutrients can occur without symptoms of intolerance. Data strongly support the use of the jejunal route based on improved gastric tolerance, lower theoretic risk of infection, lower cost, and the elimination of hyperglycemia associated with parenteral nutrition. 3 Some studies have attempted to evaluate the effect of gastric and jejunal feedings on patient outcome. Jejunal-fed subjects have significantly lower infection rates and intensive care unit stay, receive significantly higher proportions of their daily caloric intake, and have significantly greater increases in serum prealbumin and lower rates of pneumonia than patients fed by continuous gastric feeding. 14 , 29 The success of the jejuna! route for administering feedings following neurotrauma has drawn attention to achieving small bowel (jejuna!) access. Small-bore feeding tubes placed past the pyloris and ligament of Treitz, into the jejunum, allow for the delivery of enteral nutrition in patients with gastroparesis. It is commonly assumed that neuromuscular blocking agents, sedatives, and analgesics used in the treatment of neurotrauma interfere with gastric function and feeding tolerance. Postpyloric jejuna! feedings, however, are well tolerated, even during the administration of pentobarbital. 24 Spontaneous jejunal (postpyloric) feeding tube placement has recently become popular with the use of a prokinetic agent that eliminates radiologic or endoscopic intervention. Lord identified the following bedside protocol to achieve jejuna! placement: 10 mg metoclopramide intravenously, wait 10 minutes, and insert all but the last 10 inches of a 36-inch feeding tube. 22 This procedure resulted in 88% postpyloric placement within 4 hours using an 8 F unweighted small-bore feeding tube in intensive care unit patients. These findings have not been duplicated in neurotrauma patients so endoscopic or fluoroscopic guidance may be necessary if normal motility fails to migrate the feeding tube past the pyloris.
Enteral Formula Selection Because protein requirements are accentuated after neurotrauma, the protein compo-
nent is the most significant factor to consider.11 It has been suggested that initial metabolic requirements should be met while providing 15% of calories as protein as found in traditional formulas. 3 At Mission Hospital Regional Medical Center, the Metabolic Support Team advocates starting a high-protein formula such as lsosource 1.5 (Novaritis, Minneapolis, MN), a concentrated (1.5 calories per mL) formula providing 18% of calories from protein. The smaller volume of concentrated formulas is found to be better tolerated. If the patient is determined to be extremely catabolic, lsosource VHN (Novartis), providing 25% of calories as protein, is initiated. Protein content is also categorized by digestibility. Enteral formulas are available with intact protein, partially hydrolyzed protein, peptide-based protein, and crystalline amino acids, for varying degrees of digestive capacities (Table 1). Studies examining the effect of peptide-based enteral formulas indicate that they may improve visceral protein levels, such as prealbumin, and a lower incidence of diarrhea.28 Many institutions advocate the use of peptide-based formulas when feeding into the small bowel, but the high cost of these formulas and lack of documented effect on patient outcome should be considered. Ultimately, formula selection should be based on individual needs and absorptive capacity of the patient.
Targeting Caloric Requirements An accurate estimation of metabolic requirements is crucial to avoid complications of underfeeding and overfeeding. If a patient is fed insufficiently, starvation can magnify the depletion of body tissues and contribute to organ function impairment. Researchers have identified an association between multipleorgan failure and a large caloric deficit. 1Major organs deplete their structural proteins to meet the body's energy requirements to the point where the organ itself becomes inefficient and organ failure ensues. 15 In general, underfeeding delays wound healing and decreases resistance to infection. 18 The small intestine, with its large quantity of lymphoid tissue, seems to be largely responsible for immune function. It is believed to have a significant role as a protective organ by guarding against translocation of bacteria. Research in-
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PROTEIN CONTENTOF ENTERA.L FORMULAS
Type of Protein
Digestion Required
Intact protein (i11 complete and original form as found in whole foods)
Yes
Partially hydrolyzed protein
Yes
Peptide-based proteins (dipeptides and tripeptides) are proteins that have been enzymatically hydrolyzed into smaller peptide fragments
No
Crystalline amino acids
No
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BY DIGESTiBIUTY
Special Characteristics
0
For patients with normal digestive capacity and normal pancreatic enzyme activity Promotes greater stimulation of gut hormone release than amino acid formulas For patients with reduced small bowel absorptive capacity Promotes greater stimulation of gut hormone release than amino acids May be used when feeding into the small bowel May improve visceral protein levels, such as prealbumin Absorbed directly into the bloodstream via passive diffusion across intestinal mucosa (does not require sodium pump) May increase absorption of sodium and water, resulting in a lower incidence of diarrhea Requires no further digestion in the gastrointestinal tract. Requires sodium pump for active transport of nutrients across intestinal mucosa For patients with reduced small bowel absorptive capacity Adds considerably to hyperosmolality
Data from ldeno K: Enteral nutrition. In Gottschlich M, Materase L Nutritional support dietetics core curriculum, ed 2. Silver Spring, MD, Aspen, 1993, p 75; and MacBurney M, Russel C, Young LS: Formulas. In Rambeau JL, Caldwell MD Clinical Nutrition Enteral and Tube Feeding, ed 2. Philadelphia, WB Saunders, 1990.
clicates that gut function and integrity begin to deteriorate when the body is in a state of starvation. 21 For example, animal studies have determined that within 24 to 72 hours following a burn injury, the intestine becomes edematous and begins to atrophy and bacterial translocation occurs. 3°For obvious reasons, researchers are unable to duplicate this type of animal in vivo research in humans, and therefore the concept continues to be evaluated. On the other hand, overfeeding is harmful as well. Supplying too many calories can cause hepatic dysfunction, hyperglycemia, elevated levels of blood urea nitrogen (BUN), cholesterol, and triglycerides. Large amounts of glucose calories given to ventilatordependent patients can lead to an increase in C0 2 , which may impede ventilator weaning. 2 9 Planning and targeting an accurate estimation of caloric requirements is imperative for optimizing the patient's metabolic requirements.
Timing of Nutritional Support Nutritional support should be instituted within 24 hours of admission, and caloric
goals should be met within 48 hours. Because of the incidence of gastric intolerance following head injury, establishing nutritional goals quickly while simultaneously treating increased intracranial pressure can be difficult. The route of administration and formula selection should be based on individual patient need, yet a consistent approach to establishing and meeting nutritional requirements is helpful. The body can \Nithstand a short period of starvation, but we now know that recovery may be improved with the early introduction of nutritional support. It seems that delayed enteral feeding (more than 5 clays) fails to provide a reduction in complications, but early enteral feeding (less than 48 hours) is important to maintain resistance to infection. 19 Early enteral feeding has been found to be associated with improved blood flow to the intestine with preservation of gut mucosa! integrity and reduced hypermetabolic response (when compared with the parenteral nutrition). There is an abundance of evidence supporting the idea that early enteral nutrition improves recovery, decreases complications
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and infections, and improves wound healing.38 A recent study evaluated the effect of early enteral nutrition in head-injured patients when targeted caloric requirements were met on day 1. 42 There were fewer overall complications and a reduction in the postinjury inflammatory response when compared with control patients (target caloric requirements met after day 1). We may infer that patients fed enterally have better outcomes because enteral nutrition maintains the gut, an immunologically significant organ.
Administration of Nutritional Support Versus Fluid Volume Prompted by the development of "Guidelines for the Management of Severe Head Injury" in 1995 (authored by members of the American Association of Neurological Surgeons [AANS]/CNS Joint Section on Neurotrauma and Critical Care and supported by the Brain Trauma and AANS), practitioners have witnessed a significant change in practice that has had a considerable impact on the management of nutritional support. 3 The maintenance of normovolemia, which the AANS guidelines support, has eased the predicament of providing adequate calories to headinjured patients in the face of fluid restriction. Now, nutritional support is not secondary to maintaining serum osmolality and intracranial pressure. No longer must volume-restricted head-injured patients wait for days and then receive only a portion of their daily caloric requirements because of increased intracranial pressure. This change in practice has had a significant impact on the quality of nutritional support provided to head-injured patients and demands that practitioners reevaluate old practices. Maintenance of adequate nutritional support by means of preserving normovolemia alone could quite possibly be a major influence on patient outcomes following major head injury.
Monitoring Nutritional Support Nitrogen balance can be used to estimate nutritional needs and evaluate the adequacy of protein intake. A positive nitrogen balance is the goal (nitrogen intake exceeding loss), even though it is often difficult or impossible to obtain during the catabolic state. In addi-
tion, urine urea nitrogen (UUN) collections (normal range, 12 to 20 g per 24 hours) are not precise for determining nitrogen losses during the catabolic state but are useful for monitoring the extent of catabolism. A catabolic state may be identified by a negative nitrogen balance that occurs despite adequate dietary protein intake (1.5 g/kg per day). Nitrogen balance is determined by calculating the amount of nitrogen intake from the diet minus nitrogen excretion (Equation 2). Prealbumin, with a half-life of 2 days, is a biologic nutritional marker indicative of a patient's nutritional and nitrogen status. Its normal range is 10.6 to 42.4 mg/dL. Although the accuracy of prealbumin measurements is also affected by the catabolic state, it is commonly used along with indirect calorimetry and UUN to assist in guiding nutritional support supplementation. _J_I\_ useful guideline, as reported by Roberts, is to monitor prealbumin levels after 3 to 5 days on the goal rate for a given formula and weekly thereafter once it appears that metabolic needs are being met. 34 Serum mineral levels are also affected following injury, in particular, zinc, iron, and copper. Increased urinary zinc excretion has been reported in head-injured patients, which lasts up to 3 weeks. 26 · 44 Several small studies have examined the effect of zinc supplementation in head-injured patients during the immediate postinjury period. Zinc supplementation seems to be associated with improved neurologic outcome and enhanced prealbu-
Equation 2 EQUATION TO DETERMINE NITROGEN BALANCE (PROTEIN BALANCE) Protein is metabolized for energy during catabolism and must be replaced with exogenous protein to avoid protein malnutrition. The goal is to offset a loss of protein mass by infusing protein or amino acids enterally or parenterally. Values of +4 to +6 indicate an anabolic state; + 1 to -1, a homeostatic state; and less than -2, a catabolic state.
Prote~n2 ~take - (UUN excreted + 4') '4 accounts for other nitrogen losses (2 g stool g skin). UUN = urine urea nitrogen
+2
NUTRITION STRATEGIES l1N NEUROTRAUMA
min levels. 16 Zinc may be considered when scrum zinc concentrations are low.
Guidemines for Enteram INutrH:fonal Support in the Neurotrauma Patient Recent literature has outlined early enteral nutrition protocols in head-injured patients, 34 • 42 but there is little other information available to guide a standard of practice. The initiation of nutritional support following severe head injury should begin within the first 24 hours following admission. Gastric feeding is preferred because it is less expensive, and formulas can be delivered while taking advantage of the normal process of digestion and absorption. The jejuna! route should be used when gastroparesis persists, and it is often necessary in ncurotrauma during the first 4 to 5 clays postinjrny. A concentrated, full-strength formula may be attempted at a rate of 20 to 30 mL/h to evaluate tolerance. If the gastric route is successful, with or without the use of a prokinetic agent, gastric residuals should be monitored every 4 hours. If the enteral-jejunal route is achieved evidence of abdominal distention should b~ assessed. If continued evidence of gastric intolerance occurs with higher feeding rates (gastric or jejuna!), the addition of parenteral nutrition may be warranted to meet targeted caloric goals. Initially, calories should be limited to BEE X 1.0 for mechanically ventilated, pharmacologically paralyzed head-injured patients, and BEE X 1.4 for all others. Indirect calorimetry should be performed on eve1y mechanically ventilated patient by clay 5 if mechanical ventilation is anticipated to exceed 9 clays. Routine monitoring should include nutrient intake, signs of intolerance to therapy, weight changes, and biologic, hematologic, and other pertinent diagnostic data. A guideline is provided based on literature review and current practice at Mission Hospital Regional Medical Center (Appendix
CASE HISTORY A 27-year-olcl female patient was transferred to the surgical intensive care unit following a craniotomy for a large left pari-
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etal subdural hematoma that she sustained after falling from a window. Her intracranial pressure remained elevated postoperatively and required management with continuous propofol drip, analgesics, and paralytics. A nonweighted, small-bore feeding tube was placed on postoperative clay 1, and postpyloric placement was achieved within 12 hours following administration of a prokinetic agent, metoclopramide. She was started on a concentrated enteral formula at 20 mL/h (Isosource 1.5), which provided 720 calories per day. Within the following 12 hours, her goal rate was increased to 40 mL/h, providing her 102% of her estimated caloric requirements. Her initial caloric goal was set to approximate the I3EE of 1449 (based on a height of 5' 6" and weight of 140 pounds) as estimated by the Harris-Benedict equation. Fat calories provided by propofol (a lipidbased drug providing 1.1 kcal/mL) were included in the calorie count. Serum triglyceride concentration was performed before propofol administration and then followed eve1y other clay to monitor for hypertriglycericlemia. An indirect calorimetry measurement was performed on day 3, which indicated a need for 2029 kcal per 24 hours 140% above the BEE. Isosource 1.5 was i~creased accordingly (full strength) at 50 mL/h in combination with 384 mL per 24 hours of propofol, providing 2222 kcal and 13 g nitrogen, about 109% of the measured energy expenditure. Upon admission, prealbumin (13 mg/dL) was borderline low and 24-hour UUN was within normal limits (12 g per 24 hours). Serial laboratory tests indicated an increase in prealbumin on day 4, suggesting adequate nutritional clelive1y. The 24-hour UUN, however, was 15.6, resulting in a negative nitrogen balance. Because propofol was discontinued on clay 5, this allowed the dietitian to provide more calories in the form of protein, and an isotonic, highprotein formula was ordered (Isosource VHN at 85 mL/h) providing 2040 kcal and 20.2 g nitrogen, approximately 100% of both caloric and protein needs. Neurosurgical therapy to control intracranial pressure was weaned on clays 10 through 12. The patient was able to open
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her eyes, move all extremities purposefully, and follow simple commands. Indirect calorimetry was performed again, and it indicated an increase in estimated needs (2202 kcal per 24 hours), 152% of BEE. Ventilator support was discontinued on day 13, and a swallowing evaluation was performed on day 15. A dysphagic diet consisting of thickened liquids was ordered, and the patient was able to consume about
50% (1120 kcal) of her diet. Night-time enteral feedings were ordered (6 PM to 6 AM) to supplement her diet, and she was transferred from the intensive care unit on day 16. Daily calorie counts were maintained, and the patient was able to consume 75% of a soft diet by day 20 (80% of estimated caloric requirements). Enteral feedings were discontinued, and the patient continued to have steady neurologic improvement.
A basic understanding ofmetabolicalterationsthat occur following neurotrauma is essential for addressing nutritional requirements. Interventions must be rese.arch based and must focus on the support ofmetabolicalterations, miniillizing the effect of catabolism and optimizing caloric delivery to meet metabolic demand. The goal of accuracy in the delivery of nutritional support is to ensure a reduction inpatient morbidity. Nutritional support requires an ongoing, daily assessment of caloric goals, protein requirements, patient responses, and assessment of nutritional laboratory values. Using this strategy, neurotrauma patients will have the greatest opportunity for a positive outcome.
ACKNOWLEDGMENTS The authors wish to express their thanks and appreciation to the administrative, medical, and nursing staff of Mission Hospital Regional Medical Center, Mission Viejo, California. Their support of the Metabolic Support Team has made it a continuing success for over a decade.
REFERENCES 1. Bartlett RH, Dechert RE, Mault JR: Measurement of metabolism in multiple organ failure. Surgery 92:771, 1982 2. Benotti PN, Bistran B: Metabolic and nutritional aspects of weaning from mechanical ventilation. Crit Care Med 17:181, 1989 3. Bullock R, Chestnut RM, Clifton G, et al: Guidelines for the Management of Severe Head Injury. New York, Brain Trauma Foundation and American Association of Neurological Surgeons, 1995, pp 14-1-14-15 4. Cerra FB: Hypermetabolism, organ failure, and metabolic support. Surgery 101:1, 1987 5. Chiolero R, Schutz Y, Lemerch T, et al: Hormonal and metabolic changes following head injury or noncranial injury. J Parenter Enteral Nutr 13:5, 1989 6. Clifton G, Robertson C, Choi S, et al: Assessment of nutritional require1nents of head-injured patients. J Neurosurg 64:895, 1986 7. Clifton G, Roberton C, Grossman R, et al: The metabolic response to severe head injury. J Neurosurg 60:687, 1984
8. Cuthbertson DP: Alterations in metabolism following injury: Part 1. Injury 11:175, 1980 9. Dark D, Pingleton S, Kerby G: Hypercapnia during weaning: A complication of nutritional support. Chest 88:141, 1985 10. Dempsey DT, Guenter P, Mullen JL, et al: Energy expenditure in acute trauma to the head with and without barbiturate therapy. Surgery Gynecology and Obstetrics 160:128, 1985 11. Dickerson RN, Guenter PA, Gennarelli TA, et al: Increased contribution of protein oxidation to energy expenditure in head-injured patients. J Am Coll Nutr 9:86, 1990 12. Flakoll P, Wentzel L, Hyman S: Protein and glucose metabolism during isolated closed-head injury. Am J Physiol 269:636, 1995 13. Gadisseux P, Ward J, Young H: Nutrition and the neurosurgical patient. J Neurosurg 60:219, 1984 14. Graham TW, Zadrozny DB, Harrington T: The benefits of early jejuna! hyperalimentation in the heaclinjurecl patient. Neurosurgery 25:729, 1989 15. Grant JP: Clinical impact of protein malnutrition on organ mass and function. In Blackbum GL, Grant JP, Young VR (eels): Amino Acids, Metabolism and Medical Application. Boston, MA, 1990, pp 347-358 16. Harris JA, Benedict FG: A biometric study of basal metabolism in man (pub no 279). Washington DC, Carnegie Institute of Washington, 1919 17. Ideno K: Entcral nutrition. In Gottschlich I\1, ~/Iatcre:-:;e L: Nutritional support dietetics core curriculum, ed 2. Silver Spring, MD, Aspen, 1993, p 75 18. Keenan RA, Molclawer LL, Yang RD, et al: An altered response by peripheral leukocytes to synthesize or
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release leukocyte endogenous mediator in critically ill, protein-1rn1lnourished patients . .J Lah Clin Med 100:844, 1982 19. Kuclsk KA, Minard G: Enteral nutrition. In Zaloga GP (eel): Nutrition in Critical Care. Mosby, St Louis, MO, 1994, p 334 20. Lam AM, Winn R, Cullen BF, et al: Hyperglycemia and neurological outcome in patients with head injury. .J Neurosurg 75:545, 1991 21. Lord Ll'vl, Sax HC: The role of the gut in critical illness. AACN Clinical Issues in Critical Care Nursing 5:450, 1994 22. Lord Ll'vl, Weiser-Maimone A, Pulhamus M, et al: Comparison of weighted vs unweighted enteral feeding tubes for efficacy of trans pyloric intubation. JPEN J Parenter Enteral Nutr 17:271, 1993 23. Madlurney M, Russel C, Young LS: Formulas. In Rombeau JL, Caldwell MD: Clinical Nutrition: Enteral and Tube Feeding, eel 2. Philadelphia, WB Saunders, 1990 24. Magnuson B. Hatton J, Williams S, et al: Tolerance ;:incl efficacy of enteral nutrition for neurosurgical patients in pentobarbital coma. Nutrition in Clinical Practice 14:131, 1999 25. Marie C, Bratlet J: Blood glucose level and morphological brain damage following cerebral ischemia. Cerebrovascular and Brain Metabolism Reviews 3:29, 1991 26. McClain C, Twyman D, Ott L, et al: Serum and urine zinc response in head-injured patients. J Neurosurg 64:224, 1986 27. McClave SA, Sexton LK, Spain DA, et al: Enteral tube feeding in the intensive care unit: Factors impeding adequate delivery. Crit Care Med 27: 1252, 1999 28. Meredith JW, Ditesheim JA, Zaloga GP: Visceral protein levels in trauma patients are greater with peptide diet than with intact protein diet. J Trauma 30:825, 1990 29. Montecalvo J'vIA, Steger KA, Farber HW, et al: Nutritional outcome and pneumonia in critical care patients randomized to gastric versus jejuna! tube feedings: The Critical Care Research Team. Crit Care Med 20:1377, 1992 30. Moore R, Najarian MP, Konvolinka CW: Measured energy expenditure in severe head trauma. J Trauma 29: 1633, 1989 31. NortonJA, Ott LH, McClain C: Intolerance to enteral feeding in the br;:iin-injured patient. J Neurosurg 68:62, 1988 32. Ott L, Young B, Phillips R, et al: Altered gastric emptying in the head-injured patient: Relationship to feeding intolerance. J Neurosurg 74:738, 1991
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33. Rapp RP. Young B, Twyman D, et al: The favorable effect of early parenteral feeding on survival in headinjured patients. J Neurosurg 58:906, 1983 34. Roberts PR: Nutrition in the head-injured patient. New Horizons 3:506, 1995 35. Saito H, Trocki 0, Alexander JW, et al: The effect of route of nutrient administration on the nutritional state, catabolic hormone secretion, and gut mucosa! integrity after burn injury. JPEN J Parenter Enteral Nutr 11:1, 1987 36. Sacks GS, Brown OR, Teague D: Early enteral nutrition support modifies immune function in patients sustaining he;:id injury. JPEN J Parenter Enteral Nutr 19:387, 1995 37. Schlichtig R, Ayres AJ'vl: Nutritional Support of the Critically III. Chicago, IL, Year Book Publishing, 1988 38. Schroeder D, Gillanders L, Mahr K, et al: Effects of immediate postoperative enteral nutrition on body composition, muscle function, and wound healing. JPEN J Parenter Enteral Nutr 15:376, 1991 39. Spain DA, McClave SA, Sexton LK, et al: Infusion protocol improves delivery of enteral tube feeding in the critical care unit. JPEN J Parenter Enteral N utr 23:288, 1999 40. Stechmiller J, Treloar DM, Derrico D, et al: Interruption of enteral feedings in head injured patients. J Neurosci Nurs 26:224, 1994 41. Sunderland P, Heilbrun M, et al: Estimating energy expenditure in traumatic brain injury: Comparison of indirect calorimetry with predictive formulas. Neurosurgery 31:246, 1992 42. Taylor SJ, Fettes SB, Jewkes C, et al: Prospective, randomized, controlled trial to determine the effect of early enhanced enteral nutrition on clinical outcome in mechanically ventilated patients suffering head injury. Crit Care Med 27:2525, 1999 43. Varella I: Head and spinal cord injury. In Hennessy K, Orr M: Nutrition Support Nursing Core Curriculum, eel 3. Silver Spring, MD, Aspen. 1996, pp 13-7, 13-8 44. Young B, Ott L, Beard D, et al: The acute-phase response of the brain-injured patient. J Neurosurg 69 375, 1988 45. Young B, Ott L, Haack D: The effect of total parenteral nutrition upon intracranial pressure in severe head injury. J Neurosurg 67:76, 1987 46. Young ll, Ott L, Kasarskis E, et al: Zinc supplementation is associated with improved neurologic recovery rate and visceral protein levels of patients with severe closed head injury. J Neurotrauma 13:25, 1996 47. Young B, Ott L, Twyman D: The effect of nutritional support on outcome from severe head injury. J Neurosurg 67:668, 1987 Address reprint requests to Jill Donaldson, MSN, RN, CCRN, CS Vascular Institute and Stroke Center Mission Hospital Regional Medical Center 27700 Medical Center Road Mission Viejo, CA 92691
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Appendix 1. Guidelines for Enteral Nutritional Support in the Neurotrauma Patient The goal of nutritional support in the neurosurgical patient is to begin a feeding regimen within the first 24 hours following admission with the goal of achieving the targeted nutritional goal within 48 hours. A. The preference is to begin a trial of gastric feeding and to determine gastric intolerance (i.e., gastric residual of more than 150 ml) before attempting postpyloric placement of feeding tubes. However, if a small-bore feeding tube can be successfully placed at the bedside with the aid of a prokinetic agent, this initial attempt at postpyloric placement is recommended. The small-bore feeding tube should be longer than 36 inches to maintain position in the small bowel. If unsuccessful, postpyloric placement may require endoscopic or fluoroscopic guidance. Small-bore feeding tubes should be longer than 36 inches to maintain position in the small bowel. B. Maintain the head of bed at 30° or more. C. Administer prokinetic agent such as metoclopramide every 8 hours. D. A concentrated, full-strength formula may be attempted at a rate of 20 to 30 ml/h. E. If feeding into the stomach, gastric residuals must be monitored at least every 4 hours, and the rate may be increased every 4 hours up to the target goal unless gastric residuals exceed 150 ml. If gastric residual is greater than 150 ml, feeding should be held and residual should be checked in 2 hours. F. If feeding into the small bowel, obtain residuals every 8 hours (high residuals may indicate tube tip migration back into the stomach or a distal obstruction). An abdominal assessment should be performed every 8 hours. Inspect for distention and palpate for firmness. Abdominal girth may be monitored by marking the patient's skin and measuring the distance (tip to tip) between the iliac crests. Parenteral nutrition may be indicated if enteral feedings are unsuccessful.
G. If intolerance occurs (with gastric or jejuna! feeding), decrease feeding rate to 30 ml/h for 24 hours and advance as described in E. H. If long-term nutritional support is needed or anticipated to be longer than 6 weeks, alternative modes of delivery should be accessed, such as percutaneous endoscopic gastrostomy (PEG), percutaneous endoscopic jejunostomy (PEJ), jejunostomy tube CJ-tube), or indwelling catheter (for parenteral route). I. Initial calories should be limited to BEE X 1.0 for mechanically ventilated, pharmacologically paralyzed head-injured patients, and BEE X 1.4 for all others. Indirect calorimetry should be performed on every mechanically ventilated patient by day 5 if mechanical ventilation is anticipated to exceed 9 days. Routine monitoring will include nutrient intake, signs of intolerance to therapy, weight changes, and biologic, hematologic, and other pertinent diagnostic data. ]. A comprehensive nutritional laboratory panel, including comprehensive metabolic panel (Chem 20) and 24-hour UUN, prealbumin, and magnesium levels should be obtained after 3 to 5 days on the goal rate, and weekly thereafter if the nutritional laboratory panel is within acceptable limits. (UUN and prealbumin testing are not indicated for patients with renal failure.) K. Consider indirect calorimetry at days 3 to 5, and consider it weekly thereafter, especially if laboratory values or clinical condition is not consistent with initial assessment of caloric needs. L. If prealbumin is less than 10 mg/ dl, an adjustment in caloric goal or change to high nitrogen formula or both may be indicated. M. Insulin administration is indicated \vhen blood levels are elevated above 200 mg/ dl. N. If serum zinc is below normal (60 to 130 µ,g/ml), extra zinc may be adminis-
NUTRITION STRATEGIES IN NEUROTRAUivlA
tered. Zinc 220 mg oral sules, may be provided as a plemcnt. The capsules may be u1.,cu.Lu and administered through a feeding tube. If parenteral nutrition is indicated, 6 to 10 mg of elemental zinc may be added to the intravenous solutions daily. Zinc is also available in trace element combinations with chromium, copper, and manganese. 0. For transitional feeding following extubation, long-term mechanically venti-
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ideally should receive a evaluation before an appropriate diet order is prepared. P. Before discontinuation of nutritional support, the dietitian, nurse, or physician shall verify adequate oral intake. Discontinue when patient is able to resume adequate oral intake (more than sm11 of meals and supplements or more than two thirds of caloric goal) and patient is demonstrating stable nutritional parameters. ,,"""u"'·'