Nutritional Considerations

Aaron M. Cook and Barbara Magnuson Woodward

GENERAL PRINCIPLES

• Moderate-to-severe traumatic brain injury (TBI) patients often require nutrition support with either enteral nutrition (EN) or parenteral nutrition (PN) due to intubation, dysphagia, or low Glasgow Coma Scale (GCS) score.

• Controversy exists regarding optimal feeding route with respect to gastric versus small bowel delivery:

Intolerance to gastric feeding with high gastric residuals may lead to subsequent aspiration pneumonia.

Preference for duodenal or jejunal feedings often avoids gastric intolerance and optimizes EN delivery, avoiding malnutrition, and resulting immunocompromise [1–4].

• The Brain Trauma Foundation Guidelines recommend that moderate-to-severe TBI patients receive full caloric replacement by day 7 after injury (with no specification of route), and suggest initiating feeding within 72 hours after injury and targeting 100% to 140% of estimated resting metabolism expenditure (18%–25% of those calories being protein) [5].

• The American Society of Parenteral and Enteral Nutrition (ASPEN) Critical Care and Society of Critical Care Medicine (SCCM) Guidelines both recommend early EN as the initial route, and that it be initiated within 24 to 72 hours for critically ill patients [6].

DIAGNOSIS

• Clinical Presentation

TBI patients presenting with malnutrition, wounds, and other chronic disease states require an immediate nutrition assessment to optimize nutrition and minimize further malnutrition-associated complications.

Frequently reassess the ability to swallow or the need for temporary nasoduodenal (ND) or nasojejunal (NJ) feeding tube (placed at bedside) or a more secure feeding access (gastrostomy tube [G-tube]).

G-tubes are indicated when a patient presents with dysphagia for a prolonged period of time (i.e., >2–3 weeks). TBI patients are more likely to tolerate gastric feedings as the acute phase of illness subsides. Typically by week 2 or 3 after TBI, gastric administration of feedings, medications, and maintenance fluids are well tolerated.

PN should only be considered in patients with early feeding difficulty, (i.e., severe facial fractures) and inability to establish access, or who do not tolerate EN within the 4 days after injury. The benefits of early nutrition must be balanced with the high dextrose load, large fluid volume, and infectious risks of PN [7].

TREATMENT

• Guiding Principles

Prompt nutrition assessment is needed to establish goals for optimal calories, protein, and fluids.

Caution should be exercised with application of various equations utilized to predict energy expenditure that incorporate age, weight, and height.

None are specific to TBI and all have a degree of inaccuracy [6].

A weight-based equation (25–35 kcal/kg) is often utilized but again caution with obese or underweight patients should be exercised, as this lends to further the inaccuracy.

Indirect calorimetry (IC) is the current “gold standard” for accuracy of energy expenditure, but is more costly [8].

Recognize changing nutritional needs: repeating IC readings is warranted as clinical status changes, for example, immediately after TBI, as sedation and/or neuromuscular blockade is decreased, and during the convalescent phase.

Aggressively address electrolyte abnormalities:

Hypophosphatemia, hypokalemia, and hypomagnesemia develop due to intercellular shifts when carbohydrates are initiated with nutrition support.

Avoid hyponatremia and hyperglycemia.

Avoid overfeeding by accounting for the lipid caloric provision: propofol and (more infrequently) clevidipine are in a lipid emulsion solvent.

Lipids in PN regimens are often discontinued while the patient is receiving propofol.

Despite comatose appearance, TBI patients have increased metabolic needs (~120%–140% of resting metabolic expenditure) because of hypercatabolic response. Harris Benedict, Ireton-Jones 1992, Penn State 2003, and Swinamer equations are frequently utilized to determine calorie needs. Estimates may be as high as 160% in pediatric patients and adults with multitrauma [9].

Conversely, needs may be as low as 80% in pharmacologically induced coma [10].

Protein requirements range 1.2–2 g/kg depending on degree of hypercatabolism, wounds present, and if continuous renal replacement therapy is utilized.

1.5 g/kg is a typical starting protein dose.

Large volumes of salt-free water and other hypotonic fluids should be avoided to prevent exacerbation of cerebral edema or hyponatremia.

• Initial Management

Establish postpyloric feeding access as soon as possible [11].

Administer a calorically dense EN product as early as possible (preferably within 48 hours after injury) [6].

Provide at least 18% to 25% of calories as protein to account for protein catabolism.

Some studies suggest success in starting EN near goal rate; common practice tends to focus on slowly increasing EN rate to goal over 12 to 48 hours, depending on patient tolerance [12,13].

Reevaluate metabolic needs as the patient convalesces and clinically improves.

• Glycemic Control

The optimal range of glucose values is an often debated topic in critically ill individuals.

Hyperglycemia (>200–225 mg/dL) may be associated with increased morbidity and mortality in TBI patients [14,15].

The rate of infectious complications, immune dysfunction, and other noninfectious complications such as polyneuropathy are closely associated with elevated glucose levels [16].

Hypoglycemia also appears to be associated with an increased mortality in critically ill individuals [17].

TBI patients exhibit some differences in brain glucose metabolism and likely require slightly higher glucose values to ensure appropriate brain metabolism.

Maintenance of serum glucose values between 80 and 110 mg/dL (“intensive insulin”) may result in cerebrospinal fluid (CSF) glucose values below the normal threshold [18].

Serum glucose values of 100 to 180 mg/dL should result in improved CSF glucose values and reduce the risk of hypoglycemia.

• Treatment Controversies

Timing—If early is best, is “settling” for PN in first few days after injury when EN is not feasible likely to confer the same benefit as early EN?

If PN is used, clinicians should be vigilant to avoid permissive delays in EN initiation while providing early PN (i.e., should still be aggressive in attempting to start EN as soon as possible). Note that no benefits were realized with supplemental early PN in the large EPANIC trial [19].

Caution should be used in patients with intracranial hypertension or cerebral edema due to the large dextrose and fluids required in PN to meet nutritional needs.

Management of hyperglycemia—Optimal glycemic thresholds are often debated and may be different in TBI patients than in other critically ill populations.

Immunonutrition—Role of immunonutrients such as glutamine, arginine, and omega-3 fatty acids in the inflammatory response of TBI patients is ill-defined [20].

Theoretical suppositions can be made based on the pathophysiology of TBI and the mechanism of action of these immunonutrients, but clinical data are lacking.

Very few studies have evaluated combinations of pharmaconutrients in TBI patients to recommend its net benefit or harm.

Based on the current understanding of the mechanism of action of each individual nutrient, caution should be exercised when evaluating the use of immunonutrients.

Glutamine could possibly be deleterious due to the potential conversion to glutamate, an excitatory neurotransmitter known to be a major factor in the pathology of secondary brain injury, but a recent 2010 study showed this theory may not be a significant clinical concern [11].

Controversy exists as to whether arginine confers a potential net beneficial or harmful effect in TBI:

While arginine is likely beneficial for multitrauma and burn patients due to the nitric oxide–mediated perfusion and enhanced immune function, there are valid concerns for harm in TBI patients. Increasing nitric oxide in cerebral circulation may theoretically increase cerebral blood volume and intracranial pressure. Other studies, however, have shown improved cerebral blood perfusion with arginine administration early after injury [21,22].

A growing body of preclinical literature suggests that omega-3 fatty acids, specifically docosahexaenoic acid (DHA), may be able to mitigate the central inflammatory response and propagation of lipid peroxidation, due to the ischemia and metabolic dysfunction seen after severe TBI, by shunting prostaglandin production away from arachidonic acid and associated metabolites. Further clinical studies are required to validate these findings.

Optimal timing of reductions in calories and protein as the TBI patient improves clinically is not well defined. Clinicians should continue to monitor caloric needs, nutrition tolerance, and caloric intake, even after the acute illness subsides.