Nutrition
Therapeutic Goals in Acute Phase Nutrition Problems
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- Calories/Energy Needs
- Overall caloric assessment in TBI patients is determined by:
- Indirect calorimetry whenever possible, because indirect calorimetry quantifies oxygen consumption and CO2 production as determinants of energy use, which helps prevent under- and over-feeding of patients:
- Short-term (2 hr.) indirect calorimetry reliably reflects 24-hour metabolic utilization in clinically stable, sedated, ventilated patients
- Metabolic rate of patients with temperature fluctuations may vary as much as 25% in the course of a day and benefit from ongoing measurement
- Harris-Benedict equation, if indirect calorimetry is not possible, to which a stress factor of 1.4 is applied, because the Harris-Benedict equation can underestimate energy expenditure by 75% - 250%, with an average of 140%
- Guidelines for closed brain injury patients include:
- Fever and sepsis increase calories by 7.2% for every degree F above normal
- Seizures and posturing increase calories 20-30% to a maximum of 3500-4000 total calories
- Nonsedated coma increases basal energy expenditure (BEE) by 140% per Harris-Benedict
- Pentobarbital coma increases BEE by 100-120% per Harris-Benedict
- Afebrile, non-ICO patients have 120-130% increase in BEE per Harris-Benedict
- Standard head injury range is 140-200% BEE per Harris-Benedict
- Indirect calorimetry whenever possible, because indirect calorimetry quantifies oxygen consumption and CO2 production as determinants of energy use, which helps prevent under- and over-feeding of patients:
- Calories are therefore supplied at 40 - 70% above basal needs, with 30-40% as lipids to minimize hyperglycemia based, in part, on the patient's Glasgow Coma Scale score and MREE:
- Patients with GCS of 4-5 have the highest energy expenditure
- Patients who are brain dead or who are receiving sedatives, barbiturates, or musculoskeletal blocking agents have an average of 14% lower energy expenditure
- Calories can be estimated at 35 to 40 kcal/kg/d to account for the large increase in metabolic rate
- Diet and weight history, where necessary, can be obtained from family members or previous caregivers. Monitoring for hyperglycemia is necessary to prevent adverse effects.
- Overall caloric assessment in TBI patients is determined by:
- Protein needs in TBI patients are:
- Estimated at 1.5 - 2.2 g/kg of body weight; provide 2 - 2.3 g/kg of body weight as small peptides if renal function is normal. Nonsupplemented TBI patients can lose up to 10% of lean body mass in a week, up to 25% in 2 weeks, and 30-40% in 3 weeks
- Determined by estimating nitrogen losses, which can be as high as 30 g/day in acute TBI patients. Negative nitrogen balance usually persists for 2-3 weeks, regardless of the protein provided, with a peak at about 10 days postinjury. The amount of nitrogen loss correlates with:
- Serum levels of epinephrine, norepinephrine, and glucagon -- hormones associated with hypermetabolism; the more severe the injury, the greater the hypermetabolic response, and the higher the release of these hormones
- Immobility, which may potentiate nitrogen losses
- Steroid administration during the first 6 days postinjury, which further increases urinary nitrogen losses
- Provision of more protein than 1.5 - 2.2 g/kg of body weight, which results in heightened nitrogen excretion
- Amino acid patterns in TBI patients include:
- Large fluxes in alanine and glutamine, which demonstrate skeletal muscle protein release
- Lower levels of leucine, isoleucine, and valine
- Higher levels of phenylalanine
- Vitamin, mineral and fluid patterns in TBI patients include:
- Decreased plasma levels of many B vitamins and vitamin C
- Increased urinary zinc excretion/low serum zinc levels
- Salt-wasting in some patients
- Phosphorus, potassium, and magnesium decreases in some patients with the initiation of feeding
Supplementation with vitamins and minerals is recommended if the nutrition regimen falls below the Recommended Dietary Allowances (RDAs).
- Lipids - Provide a lipid source with 50-70% medium-chain triglycerides and an omega-3 ratio of 2:1 to 8:1 (Twyman, 1997)
- Methods of nutritional support - The most appropriate route for nutritional support in TBI patients must be assessed based on concurrent abdominal trauma:
- Enternal Nutrition
- Nasoenteric tubes are used for short-term feeding in patients without risk of pulmonary aspiration from gastroesophageal reflux; orogastric tubes are used if facial trauma proscribes nasal tube passage
- Jejunal tubes (J-tubes) are frequently placed during laparotomy to allow early enteral feeding in patients with high gastric residuals/delayed gastric emptying and/or dysphagia. Advantages over gastric feedings in these patients include:
- A greater number of calories are delivered
- Full caloric delivery is attained in approximately 4 days
- Improved nutritional status is achieved
- Gut immune function is stimulated and deterioration of intestinal integrity/concomitant sepsis are prevented
- Decreased stress response, a lower incidence of GI aspiration, and decreased intestinal permeability to toxins are made possible
- Parenteral Nutrition
- Appropriate method if it is unsafe to use the GI tract, the GI tract is nonfunctioning, or enteral access is unobtainable
- Component mixture should include amino acids, fats, and carbohydrates
- Routine complications of TPN, such as hypophosphatemia, hyperphosphatemia, hypomagnesemia, hypermagnesemia, hypokalcemia, hyperkalcemia, and hyperglycemia, may be increased by the fluid and electrolyte abnormalities commonly seen following TBI
- Daily, aggressive monitoring is necessary and conversion to enteral nutrition at the earliest possible time is recommended.
- Enternal Nutrition
Based on information in Matarese LE and Gottschlich MM. Contemporary Nutrition Support Practice; A Clinical Guide. Philadelphia: Saunders, 1998; Mahan LK and Escott-Stump S. Krause's Food, Nutrition, & Diet Therapy, 9th ed. Philadelphia: Saunders, 1996; and Rombeau JL and Rolandelli RH, eds. Enteral and Tube Feeding, 3rd ed. Philadelphia: Saunders, 1997, except for information where other papers are cited.

