Nutritional Care of the Spinal Cord-Injured Patient

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Chapter 184 Nutritional Care of the Spinal Cord–Injured Patient

Spinal cord injury (SCI) is a devastating and life-changing event that often results in significant morbidity and potential mortality. A multidisciplinary team approach consisting of surgeons, critical care intensivists, rehabilitation physicians, nurses, therapists, and dietitians is helpful to both the initial and long-term management of these challenging patients. In addition to recent advances in technology and surgical techniques, there have been significant medical advances in the management of patients with SCI. Nutritional optimization of these patients is one such critical element because malnourishment increases the risk of infection and potentially limits the recovery of the affected individual. This chapter provides an overview of the unique metabolic demands and nutritional support strategies in the SCI population.

Estimation of Nutritional Requirements

Prediction of Calorie Requirements

An accurate determination of the metabolic profile of each patient is necessary in the initial evaluation of patients with SCI. A variety of factors such as age, sex, level of injury, and medical comorbidities must be considered.1 Inaccuracy in calculating patient metabolic requirements could lead to either underfeeding or overfeeding, both of which can be detrimental to the patient. 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 CO2 production, and ventilator weaning difficulties.

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). A variety of factors, including age, sex, body surface area, and fasting versus fed states, directly affect BEE.1 The Harris-Benedict equation is the most common method used to estimate this energy requirement. This formula requires weight to be measured in kilograms, height in centimeters, and age in years.2 As shown in the following equations, BEE is calculated differently for men (BEEm) and women (BEEw):

(1) image

As previously mentioned, critically ill patients 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 by either an activity factor (1.2 for bedrest) or a stress/injury factor (1.6 to 1.75 for major trauma).3,4 In the patient with SCI, this posttraumatic hypermetabolic and hypercatabolic state is superimposed on a state of muscle inactivity caused by paralysis. Therefore, the use of the usual activity factor of 1.2 for bedrest may overestimate caloric needs and result in excessive delivery of calories.3,57

Factors That May Escalate Energy Expenditure

Major traumatic injury such as SCI increases the metabolic rate and has been described as “sudden stimuli to which the organism is not quantitatively or qualitatively adapted.”6 The extensive multisystem trauma and long bone fractures that commonly occur in association with SCI can augment this hypermetabolic response.8

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.9 However, some conditions such as pancreatitis, a relatively common complication of SCI,10,11 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. However, the loss of sympathetic innervation and the inability of muscles to shiver can lead to wide changes in basal metabolic rates.1214 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 because they are not performing spontaneous breathing. Critically ill patients who are sedated and relatively motionless exhibit an even lower energy state.15

Although the Harris-Benedict equation does account for 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. Therefore, the more complicated the patient, the poorer the ability to predict metabolic rates based on these equations and formulas. Actual energy expenditure measurements represent a more sophisticated and complete assessment of the patient with SCI.

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.16 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 very precise, it is neither practical nor feasible for acutely traumatized patients with SCI. However, the commonly used equations to predict resting metabolic rate overestimate this rate in patients with SCI by 5% to 32%.17 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.

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.16 The basis for this calculation is that oxygen consumption (image) and carbon dioxide production (image) 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,18 as explained in the following equation:

(2) image

An additional feature of the metabolic cart is the ability to calculate not only the REE, but the respiratory quotient (RQ) from the measured image and image. The RQ is the ratio of image/image, and can be used as an indicator of substrate use.16 Each energy source (carbohydrate, protein, and fat) is oxidized at a known RQ, ranging from 0.7 to 1 (Table 184-1). 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.

TABLE 184-1 Respiratory Quotient (RQ) Depending on Substrate Used

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.1926 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.5,20,2733 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.34

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.3 Kearns et al.29 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.29 Young et al.35 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.35 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.3,32,36 This obligatory negative nitrogen balance is not corrected with increased caloric intake.32

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.3,28,29,32,37 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 et al.,38 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 et al.,30 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.30

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.5,7,20,27,33 By studying 22 patients with SCI at more than 2 months after injury, Cox et al.20 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.20 Mollinger et al.7 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. Clarke5 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 Laventure33 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.1 Female sex and lower levels of injury were both associated with lower calorie intake and BMI. Using the SCI-adjusted BMI (recommended <22 kg/m2, overweight 22–25 kg/m2, and obese >25 kg/m2), 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.

Basic Nutritional Requirements

Carbohydrate Requirements

Glucose is the preferred energy substrate for CNS tissue, blood cells, granulation tissue, testes, and renal medulla. A minimum of 100 to 150 g/day of glucose is required for their basic function as well as for the prevention of excessive protein breakdown.39 The rate at which the body oxidizes carbohydrate or glucose is approximately 2 to 4 mg/kg/min under normal conditions. During severe stress, the oxidation rate of glucose is elevated to 3 to 5 mg/kg/min. In most patients, the provision of more than 400 to 500 g/day of glucose exceeds the body’s ability to oxidize it and use it for energy. The excess glucose is converted to fat and can be measured by calorimetry as an increased image/image ratio (increased RQ).19 Despite the CNS’s need for glucose, patients with chronic SCI have been shown to have glucose intolerance due to insulin resistance.40

The relationship between derangements in glucose metabolism and neural injury has been studied extensively, especially with regard to ischemia.4145 The results of these studies suggest that hyperglycemia at the time of, and immediately after, neurotrauma (including SCI) may worsen outcome. High serum glucose levels increase the substrate available for anaerobic glycolysis, and thus for the production of lactic acid.46 CNS lactic acid production may have an adverse effect on the recovery from neurologic injury.47 Control of serum glucose levels (i.e., prevention of hyperglycemia), especially during the first 2 to 8 hours postinjury, appears to be crucial for optimal recovery. However, increased glucose availability may be advantageous after 2 to 8 hours postinjury, and early calorie supplementation can then be implemented.47

Lipid Requirements

After glucose is stored, the body preferentially resorts to lipid metabolism rather than depleting protein stores.48 Provision of lipid as a concentrated source of calories can facilitate protein sparing, decrease the risk of carbohydrate overfeeding, and help limit total fluid volume. Fat should generally constitute 30% of the total calorie delivery. In the acute postinjury stage, large amounts of fat (>30%), especially linoleic or omega-6 fatty acids, can have an immunosuppressive effect by stimulating the release of arachidonic acid.39 This precursor leads to prostaglandin formation and subsequently depresses cell-mediated hypersensitivity, lymphocyte proliferation, and natural killer cell function. High serum triglyceride levels also indicate fat intolerance and the need to reduce the amount of intravenous lipid emulsions delivered. A minimum of 4% of total energy needs should be provided as essential fatty acids to avoid deficiency.39



Alterations in calcium metabolism after acute SCI have been well documented.8,52,53 Bone homeostasis represents a balance between bone destruction and building. After SCI, the skeleton is often no longer capable of carrying and supporting the body. This state of effective immobilization causes bone reabsorption below the level of injury beginning within 10 days of injury and lasting for at least 6 months.54,55 This may lead to high serum and urine calcium levels. Adults are susceptible to hypercalcemia because of impaired renal function and excretion difficulties, whereas children may have hypercalcemia because of increased bone turnover rates.40,56 Although rare after SCI, symptoms of hypercalcemia include anorexia, nausea and vomiting, abdominal cramps, constipation, headache, and lethargy.

A low-calcium diet does not appear to be effective in decreasing serum calcium levels.57 Ultimately, this negative calcium balance leads to osteoporosis in all skeletal structures below the lesion. Ragnarsson and Sell58 showed, in a retrospective study, that the incidence of lower extremity fractures is greater in paraplegic patients than in quadriplegic patients. This is believed to be due to higher activity levels in the former group. Most of these fractures occurred in osteoporotic bones, without known trauma or after trivial injuries.58

Women with SCI have decreased bone density and increased fracture risk compared with healthy control subjects.59 Increased bone resorption rate, low parathyroid hormone levels, and low vitamin D levels are some contributing factors. Aggressive therapies to treat and prevent osteoporosis in patients with SCI include adequate nutritional supplementation (especially calcium and vitamin D intake), bisphosphonates, estrogen (in postmenopausal women), weight bearing, and functional electrical stimulation.


Anemia is a common complication of acute SCI, even in the absence of significant blood loss.50,60 Huang et al.,60 in a study of 28 patients with acute SCI, found normochromic, normocytic anemia in 71% and normochromic, microcytic anemia in 14%. They speculated that iron deficiencies, immune system changes that alter bone marrow maturation, and the effects of stress were causative factors. The process of erythropoiesis was not found to be altered in patients with SCI.60

Anemia associated with chronic disorders, such as decubitus ulcers or urinary tract infections, was the most common type discovered in patients with chronic SCI studied by Perkash and Brown.61 Anemia has also been identified as a factor related to increased length of stay for patients admitted to rehabilitation centers.62 Recognition of the potential causes of anemia might speed the rehabilitation process.


The prevalence of hyponatremia in patients with acute SCI is reportedly much higher than in general surgical populations.63,64 The strongest predictor of the development of hyponatremia is the extent of neurologic injury. The highest risk is observed in patients with complete motor and sensory SCI. Low serum sodium levels (<135 mM/L after correction for hyperglycemia) usually occur within the first week postinjury. Possible mechanisms include increased fluid intake, intrarenal defects in water excretion, resetting of the osmostat, and excessive sodium losses.65


Evidence of inadequate vitamin intake in patients with SCI has been well documented in recent studies.6668 In a cross-sectional study by Walters et al.,66

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