Summary of Key Points
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An individualized multidisciplinary team approach regarding a nutritional and activity plan is necessary during the acute, rehabilitation, and community phases of the treatment of patients with spinal cord injury.
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For optimal patient outcome, a complete nutritional assessment including age, sex, level of injury, medical comorbidities, and activity level must be performed and reassessed frequently during each setting.
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The Harris-Benedict formula for estimation of basal energy expenditure should only be used when direct or indirect calorimetry is unavailable, as it may overestimate needs.
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Patients with pressure ulcers and infection have increased protein and micronutrient requirements.
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Patient and caregiver education as well as support accessing resources are essential for nutritional and activity plan implementation.
Spinal cord injury (SCI) is a devastating and life-changing event that affects individuals with unique health backgrounds, anthropometric measurements, and personal goals and expectations. An individualized, multidisciplinary team approach consisting of surgeons, critical care intensivists, rehabilitation physicians, nurses, physical and occupational therapists, and registered dietitians is necessary in the acute, rehabilitation, and community settings of these challenging patients. Nutritional optimization of these patients is critical because malnourishment increases the risk of infection, diminishes quality of life, and potentially limits the recovery and life span of the affected individual. This chapter provides an overview of the dynamic metabolic demands and nutritional support strategies in the adult SCI population. In addition, we have integrated established guidelines and recent approaches to nutritional evaluation and treatment recommendations for those with SCI.
Estimation of Nutritional Requirements
Prediction of Calorie Requirements
A complete nutritional assessment of each patient is necessary in the acute care setting after SCI. A variety of factors such as age, sex, level of injury, and medical comorbidities before and after the injury must be considered. Patients with digestive, cardiovascular, pulmonary, or renal system disorders have specific issues that affect every aspect of their nutritional needs. For example, patients with chronic SCI require increased vitamin, mineral, and complex carbohydrate intake and decreased fat intake. High levels of fat intake, low intake of dietary fiber, nominal activity levels, and a predisposition to the development of cardiovascular disease place patients with SCI at an increased risk for cardiopulmonary morbidity and mortality. In addition, anthropometric measurements including weight, height, waist and hip circumference as well as other factors including prior nutrition-related history, nutritional labs, and swallowing abilities alter the ultimate nutritional care plan.
Inaccuracy in calculating patient basal metabolic requirements could lead to either underfeeding or overfeeding, both of which can affect the body’s ability to sustain physiologic mechanism. Underfeeding results in muscle wasting, decreased immunocompetence, and poor wound healing. Overfeeding, however, is associated with fluid overload, hyperglycemia, elevated blood urea nitrogen (BUN), elevated triglyceride levels, abnormal hepatic enzyme levels, respiratory distress caused by increased CO 2 production, ventilator weaning difficulties, and delay in functional improvement
Standard Nutritional Requirement Formulas
The energy required to fuel basic life processes in healthy, resting, fasting individuals is defined as the basal energy expenditure (BEE) or basal metabolic rate (BMR). A variety of factors, including age, sex, body surface area, and fasting versus fed states, directly affect BEE. A balance between daily intake and caloric expenditure has been studied in patients with SCI, and although the Harris-Benedict equation is the most common method used to estimate this energy requirement, some feel it cannot accurately predict the BEE in the SCI population (Kahill 2013). This formula requires weight to be measured in kilograms, height in centimeters, and age in years. As shown in the following equations, BEE is calculated differently for men (BEE m ) and women (BEE w ):
BEE m = 66 + ( 13.7 × weight ) + ( 5 × height ) − ( 6.8 × age ) BEE w = 655 + ( 9.6 × weight ) + ( 1.7 × height ) − ( 4.7 × age )
Critically ill patients with spinal cord injury require more energy than indicated by their BEE. This additional energy requirement is termed the predicted energy expenditure and is estimated by multiplying the BEE using the admission weight by either an activity factor (e.g., 1.1 for bed rest) or an appropriate stress/injury factor (e.g., 1.2 or 1.6 to 1.75 for SCI or major trauma, respectively). In the patient with SCI, this posttraumatic hypermetabolic and hypercatabolic state is superimposed on a state of muscle inactivity caused by paralysis with differences noted between those with tetraplegia versus paraplegia. Therefore, the use of the activity factor of 1.1 for bed rest may still overestimate caloric needs and result in excessive delivery of calories.
Factors That May Alter Energy Expenditure
Major traumatic injury such as SCI initially increases the metabolic rate and has been described as “sudden stimuli to which the organism is not quantitatively or qualitatively adapted.” The extensive multisystem trauma and long bone fractures that commonly occur in association with SCI can augment this hypermetabolic response. Over time, a decrease in energy expenditure is expected secondary to the lack of physical activity, reduced fat-free mass, and the lower sympathetic nervous system activity. Inability to shiver has been described in this patient population, which is believed to also be associated with the loss of sympathetic innervation and associated with wide changes in basal metabolic rates. A patient with SCI therefore requires regular reassessment of caloric needs during the all stages after injury.
Postinjury hypermetabolism is a cascade response caused by the hormonal effects of increased glucagon, cortisol, and catecholamine levels. There is a small decrease in plasma thyroxine with SCI, but this does not appear to influence the metabolic rate. However, some conditions such as pancreatitis, a relatively common complication of SCI, can significantly increase energy expenditure.
Increase in body temperature after SCI is a common phenomenon and frequently the result of a pulmonary or urinary tract infection. The degree of temperature regulation impairment is also proportional to the extent and spinal level of the paralysis. In addition, greater fluid retention and subsequent increased body weight result in falsely elevated predictions. Ventilated patients do not require as much energy if they are not performing spontaneous breathing. Critically ill patients who are sedated and relatively motionless exhibit an even lower energy state.
Again, although the Harris-Benedict equation does allow for differences in activity and the metabolic stress/injury response, there are certain deficiencies in its use. For instance, other critical factors such as infection, body temperature, nutritional support regimens, clinical procedures, surgical operations, and medications are omitted. Patient variability regarding these factors can complicate the use of predictive equations for energy expenditures. Studies have shown that the basic metabolic rate was overestimated in patients with SCI by 5% to 32%. Specifically, measurements of resting metabolic rates in patients with SCI are 14% to 27% lower than their healthy counterparts because of decreased fat-free body mass and baseline sympathetic activity. Therefore, the more complicated the patient, the poorer the ability to predict metabolic rates based on these equations and formulas. Actual energy expenditure measurements, such as direct or indirect calorimetry, represent more sophisticated and complete assessments of patients with SCI. As we will fully describe, the Harris-Benedict formula should only be used when direct or indirect calorimetry is unavailable.
Calorimetry: Measurement of Energy Expenditures
Calorimetry is a more accurate technique to determine energy expenditure. Unfortunately, it is more expensive and requires precision equipment and appropriately trained personnel. Nevertheless, energy expenditures can be accurately determined by using either direct or indirect calorimetry.
Direct calorimetry measures heat production or heat loss by the body. To obtain these measurements, a subject is placed in a sealed chamber with a supply of oxygen. Because the chamber is well insulated, the heat produced by the body is absorbed by a known volume of water that circulates through pipes located in the chamber. The change in water temperature reflects the person’s heat loss and represents expended metabolic energy. Although this method is precise, it is neither practical nor feasible for acutely traumatized patients with SCI.
Indirect calorimetry is a more useful and accurate alternative to the direct method. This technique is used to measure energy expenditure in critically ill patients. Heat production or resting energy expenditure (REE) is determined with a metabolic cart (Critical Care Monitor, Medical Graphics Corporation, St. Paul, MN) by measuring respiratory gas exchange between the inspired and expired samples. The basis for this calculation is that oxygen consumption ( 
) and carbon dioxide production ( 
) accurately reflect a significant portion of systemic intracellular metabolism. The REE is determined from the data obtained by the metabolic cart study and the Weir equation, as explained in the following equation:
REE = ( 3.9 [ V ˙ O 2 ] + 1.1 [ V ˙ CO 2 ] ) 1.44
An additional feature of the metabolic cart is the ability to calculate not only the REE but the respiratory quotient (RQ) from the measured 
and 
. The RQ is the ratio of 
, and it can be used as an indicator of substrate use. Each energy source (carbohydrate, protein, and fat) is oxidized at a known RQ, ranging from 0.7 to 1 ( Table 199-1 ). Therefore, the RQ can be used occasionally to determine the predominant substrate used. For example, when the measured RQ is greater than 1, lipogenesis is assumed to occur. Substrate adjustments can be made in the nutritional support regimen based on the useful information acquired from the metabolic cart study.
| Substrate Used | RQ |
|---|---|
| Ethanol | 0.67 |
| Fat | 0.71 |
| Protein | 0.82 |
| Mixed substrate oxidation | 0.85 |
| Carbohydrate | 1 |
| Ketone bodies | 1 |
| Lipogenesis | > 1 |
Overview of the Metabolic Stress Response
Major Trauma, Surgery, and Sepsis
After acute SCI, the patient enters a hypermetabolic and hypercatabolic state. This phenomenon is similar to that seen after trauma, major surgical interventions, and sepsis. This hypermetabolic and hypercatabolic state results in a remarkable increase in energy expenditure, total-body protein catabolism, and nitrogen excretions. The energy requirements of the trauma patient, often in excess of 200% of BEE, are necessary to maintain lean body mass. If the nutritional requirements are not met from exogenous sources, the body will use internal sources, such as body fat and muscle reserves. For example, increased protein turnover indicates that postinjury caloric requirements are much higher than maintenance levels. This accelerated protein breakdown results in a supply of amino acids for the gluconeogenesis that is needed to fuel anaerobic glycolysis in the injured tissues.
There are numerous metabolic variables in the critically ill patient that deserve close scrutiny. Hypervigilance to the nutritional status of these patients helps prevent the detrimental consequences of depleted muscle mass, increased susceptibility to infections, and impaired wound healing. The patient with SCI differs from other patients in that the neuronal disconnection of the muscles causes a decrease in muscle use and compensatory atrophy, thus lowering the energy expenditure. In addition, there are two unique metabolic responses to SCI superimposed on this already complex pathophysiologic process: an acute nutritional response and a delayed nutritional response.
Acute Nutritional Response to Spinal Cord Injury
In the acute period after SCI, which we define as less than 4 weeks postinjury, the patient’s metabolic response is influenced by the hypermetabolism related to the traumatic injury, as well as by the decreased energy requirements related to the muscle paralysis. The degree of neuronal injury resulting in loss of muscle stimulation and atrophy has been directly correlated with REE. Therefore, a quadriplegic patient has a lower energy expenditure than a paraplegic patient, whose energy expenditure in turn is less than that of a patient without SCI.
Actual REEs, measured by indirect calorimetry during the first and second weeks after SCI, have demonstrated that calorie needs are overestimated when the Harris-Benedict equation for BEE (see Equation 1 ) is used in conjunction with injury and activity factors. Kearns and colleagues also reported that the average REE after acute SCI was lower than predicted by the Harris-Benedict equation for BEE. They hypothesized that nonspecific changes in neurogenic stimuli and decreased oxygen consumption by flaccid muscles contributed to these findings. Their hypothesis was further supported by the observation that the REE increased by 5% as muscle tone returned. Young and associates excluded the injury and activity factors used in the Harris-Benedict equation for predicted energy expenditure in four patients with acute SCI, despite their traumatic injuries. The result of this calculation, which was significantly lower because of the loss of activity and trauma factors and additional factor adjustments, was determined to be 97% of the predicted value using indirect calorimetry. This emphasizes the inaccuracy and elevation of the predicted energy expenditure obtained using standard formulas and equations for the patient with acute SCI. These patients also have persistent negative nitrogen balance during the first 3 weeks after injury despite aggressive nutritional replacement. This obligatory negative nitrogen balance is not corrected with increased caloric intake.
Delayed Nutritional Response to Spinal Cord Injury
Resolution of the hypermetabolic and hypercatabolic states after SCI occurs between the third and fourth weeks postinjury. The patient then enters the delayed nutritional response to SCI. This change in metabolism is indicated by resolution of the negative nitrogen balance. Several investigators have reported that the delayed metabolic response to SCI is marked by a reduction in energy expenditure of up to 67% and is associated with a progressive loss in lean body mass. Agarwal and colleagues, in a study of 15 quadriplegic patients at a mean of 9.2 years after injury, found that measured energy expenditures were markedly lower than calculated expenditures based on the Harris-Benedict BEE. The results of this study illustrated that the delivery of calories based on the Harris-Benedict formula leads to overfeeding. This was further demonstrated by Kearns and coworkers, whose five chronic quadriplegic patients showed that the BEE as calculated using the Harris-Benedict equation exceeded energy expenditure by a factor of 1.5. Although the time frame of this study in relation to injury was not specified, they suggested reducing the estimated number of calories by 20% in the patient with chronic SCI.
The reduced caloric needs of patients with SCI appear to be proportional to the spinal level of the neurologic lesion or the mass of denervated muscle. By studying 22 patients with SCI at more than 2 months after injury, Cox and associates showed that quadriplegic patients required 22.7 kcal/kg/day, whereas paraplegic patients required 27.9 kcal/kg/day. They further noted that upon allowing uncontrolled diets, patients gained on average 1.7 kg per week. Mollinger and coworkers also confirmed the lower caloric needs of patients with SCI compared with the calculated BEE, as well as a significant correlation of energy expenditure with the level of the spinal cord lesion. Clarke concluded that metabolic data obtained from healthy subjects could not be used to predict caloric expenditures in paraplegic patients, even when allowances were made for body weight. Sedlock and Laventure attributed this discrepancy to the loss of lean body mass after paralysis.
Total calorie intake, nutrient consumption, and body mass index (BMI) were investigated in a cross-sectional study of 73 patients with SCI with respect to sex and level of injury. Female sex and lower levels of injury were both associated with lower calorie intake and BMI. Using the SCI-adjusted BMI (recommended < 22 kg/m 2 , overweight 22 to 25 kg/m 2 , and obese > 25 kg/m 2 ), 74% of the patients were overweight or obese. Therefore, clinicians should consider adjusting BMI for the SCI population to better determine the risk of obesity and associated comorbidities in these patients.
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