Elmer

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ress

J Clin Med Res • 2012;4(4):227-236

Malnutrition in Spinal Cord Injury: More Than
Nutritional Deficiency
Yannis Dionyssiotis

Abstract
Denervation of the spinal cord below the level of injury leads tocomplications producing malnutrition. Nutritional status affects
mortality and pathology of injured subjects and it has been reported
that two thirds of individuals enrolled in rehabilitation units are
malnourished. Therefore, the aim should be either to maintain an
optimal nutritional status, or supplement these subjects in order toovercome deficiencies in nutrients or prevent obesity. This paper reviews methods of nutritional assessment and describes the physiopathological mechanisms of malnutrition based on the assumptionthat spinal cord injured subjects need to receive adequate nutrition
to promote optimal recovery, placing nutrition as a first line treatment and not an afterthought in the rehabilitation of spinal cord
injury.
Keywords: Spinal cord injury; Malnutrition; Obesity; Physiopathology; Rehabilitation

Introduction
During the last 50 years the medical world has becomeaware of the effectiveness of early, aggressive nutrition in
reducing complications in spinal cord injury (SCI). Specific dietary approaches are indicated for this population toachieve optimal nutritional status [1, 2]. Nevertheless, nutritional deficiency in a hospital setting is still a common issue,
despite the advances in medical and nutritional science. Surveys show that 40-50% of patients admitted to hospitals are
at risk of nutritional deficiency and up to 12% are severely

Manuscript accepted for publication April 30, 2012
Medical Department, Rehabilitation Center Amyntaio, General Hospital of Florina, 2nd km National Road Amyntaio-Thessaloniki, 53200,
Amyntaio, Florina, Greece. Email: yannis_dionyssiotis@hotmail.com
doi:10.4021/jocmr924w

malnourished [3, 4]. On the other site, studies report a variable prevalence of obesity from 40 to 66% in persons withSCI completing the spectrum of malnutrition [5-8]. In subjects with SCI particular attention should be paid to the metabolic differences in the nutritional status in order to optimize
the medical and neurological benefits. After the injury, well
documented hyper catabolic responses may lead to deleterious effects such as loss of lean body mass, obesity, increased
susceptibility to infections, and reduced wound healing [5,9]. The paralysis and loss of function that usually occur after a SCI produce additional metabolic and nutritional deficiencies with tetraplegics being at higher risk of malnutrition
than paraplegics [10, 11]. SCI subjects lose muscle mass andbone and gain fat mass especially below the level of injury.
Unwanted weight gain should be prevented because induces
the risk for diseases such as diabetes, coronary heart disease
and dyslipidaimias in this population [9]. According to theabove the term malnutrition includes not only under nutrition
but also over nutrition/obesity. The optimal nutritional assessment and management of the spinal cord injured subject canminimize the complications associated with acute traumatic
injury and long-term rehabilitation [12]. This paper reviews
methods of nutritional assessment and describes the physiopathological mechanisms of malnutrition in SCI subjects.

Nutritional Assessment
No single parameter can continually assess the nutritional
status or provide the effect of diet in preventing and treatingcomplications. For an initial assessment of nutritional status serial measurements to assess trends over time and thenmonitor the response to a dietary intervention may be useful.
The proposed assessments should be interpreted collectively
including the examination of possible factors that contributeto the nutritional status, such as age, sex, over-or under-hydration, interactions between drugs-food, metabolic stress,
infection, and the existence of other diseases [13].
Diet history
Adequate intake of nutrients is intercepted by many factors,

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Dionyssiotis

J Clin Med Res • 2012;4(4):227-236

Table 1. Classifications Based on the Weight for BMI and Obesity Category [3]Classification

BMI (kg/m2)

Obesity Category

Underweight< 18.5-

Normal18.5 - 24.9-

Overweight25.0 - 29.9-

Obesity30.0 - 34.9

I

Moderate obesity

35.0 - 39.9

II

Extreme obesity> 40.0III

such as difficulty in chewing and swallowing, difficulty inobtaining and preparing food, immobility, negligence, depression, and anorexia. Assistance during meals may beneeded if SCI subjects are not in a position to feed by themselves, but using adaptive equipment they can become more
independent [8]. Moreover, gastrointestinal function is compromised: gastric dilatation and paralytic ileus occurs often,
although the intestinal activity usually returns within the firstweek after injury. For patients with dysphagia or strictureof the esophagus soft food usually improves the nutrient intake. Constipation can be prevented with adequate dietaryfiber and fluids while rates of gastric evacuation are normal,
regardless of level or complete or incomplete nature of thelesion [14].
Nutritional requirements
The provision of energy and nutritional requirements is avery important factor for patient management. Malnutrition,in this case under or over nutrition, can lead to muscle loss,
atrophy of the lining of the intestine, immunochemical reduction, poor wound healing and fluid overload, hyperglycemia, high levels of urea nitrogen in blood, high triglycerides,
elevated liver enzymes, respiratory exhaustion due to increased production of CO2, and difficulty weaning from theoxygen, respectively. The assessment of nutritional requirements includes not only calculations but also the opinion ofan expert clinician in order to assess the clinical and morphometric data before applying the equations that provide
the energy and protein requirements [15].There have been
several methods for predicting energy expenditure (EE); thecomponents and the methods for its determination and estimation, summarizing their main advantages and limitations
have been recently reviewed [16]. However, because of various confusing factors such as infections and sepsis, hyper
nutrition supportive nutritional diets, clinical procedures,
postoperative medications, and changes in body weight such

228

as sarcopenia, obesity, amputations and significant weight
loss, the prediction equations can be complex and invalid[17]. Basic energy expenditure (BEE) is estimated by theequation of Harris-Benedict (HBE), while BEE is calculated
by sex with the following formula: Men: 66.5 + 13.8 (wt)
+ 5.0 (ht) - 6.8 (age), Women: 655.1 + 9.6 (wt) + 1.8 (ht)
- 4.7 (age), where wt is the weight in kilograms and ht isheight in meters, is considered as the standard criterion inpredicting caloric requirements of patients in the acute phaseof the disease for many years, although it may overestimate
energy needs [18, 19]. Predicted energy expenditure (PEE)
is calculated as follows: (BEE) x (activity rate) x (the agentof injury), while activity rate (an activity factor for bed rest)
and agent of injury (an injury factor for major trauma) are
1.2 and 1.6, respectively [20].
Assessment of subjects in the clinical setting
Patients admitted in the hospital should be examined for actual or potential occurrence of malnutrition because of anunintentional weight loss or gain. In the clinic this examination includes measurements of body weight depicting a lossof more than 10% of normal body weight within 6 months orloss of more than 5% of usual body weight within 1 month or
20% more or less than ideal body weight (IBW), calculationof body mass index (BMI) < 18, depletion of visceral protein(serum albumin < 3.5 g/dl, serum transferrin < 200 mg/dl,
serum cholesterol < 160 mg/dl, serum pre-albumin < 15 mg/
ml, creatinine height index (CHI) < 75% (measured by 24hour creatinine excretion, which is typically associated withmuscle mass of the patient as an indicator of malnutrition,
especially in young men), and the presence of diet modifications (patient receives total parenteral nutrition (TPN) or enteral nutrition (EN), inadequate food intake due instructions
for stopping any food by mouth (NPO), liquid diet, disordersof absorption, reduced swallowing capacity, increased metabolic needs, gastrointestinal disturbances (nausea, vomiting,

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Malnutrition in Spinal Cord Injury

J Clin Med Res • 2012;4(4):227-236

Table 2. Basic Levels of Albumin and Nutritional Status Distribution
Albumin (g/dl)

3.5 - 53 - 3.5

< 3.5

< 3.0

< 2.5

Nutritional
statusnormalPoint that
dietaryintervention
should berevised or
adjusted.

Associated withpoor outcomeof surgery,rising costs of
hospitalizationand prolonged
stay in ICU.

Severemalnutrition

Increased
morbidity andmortality.

diarrhea, constipation). Unintentional weight gain is an increase in body weight that occurs when a person takes inmore calories than the body needs or uses [21].
Anthropometric evaluation
For able bodied persons the World Health Organization(WHO) advocates use of BMI as a population-level indicator of obesity which is not a direct measure of body fat, but amore accurate indicator of overweight and obesity than relying on weight alone. BMI is calculated using the equation
weight (Kg)/height (m2), which is a very practical and usefulmeasure that allows the easy determination of categories ofweight status. In able bodied subjects overweight is defined
as a BMI of 25 - 29.9 kg/m2 and obesity as a BMI of ≥ 30.0kg/m2 (Table 1). In chronic spinal cord injured patients it
measuring fat with BMI is not enough to determine subject’s
percentage of fat in the body (see discussion) [9, 22].
Anthropometric standards such as the ideal body weight(IBW), the triceps skin fold thickness and the middle arm
circumference which are common tools for assessment of
nutrition may not be valid for patients with spinal cord injury due to water changes, atrophy of muscles because ofimmobility, increased body fat, and the inevitable weightloss beyond the normal. Patients’ early weight loss is mainly
due to loss of muscle rather than fat which bias the resultsof validity. In chronic paraplegics, the ideal weight has been
estimated to be 4.5 to 6.5 kg below their respective controls
finding which is in line with our recently published results[9]. Indeed, height and weight measurements are the key elements in nutritional assessment. The IBW is determined by
the height. No matter which method of calculation is used,
the IBW should be adjusted for body type (frame sizes: small- IBW 10% reduction, middle size - no changes required,large size - IBW increased by 10%) and spinal cord injury(paraplegia - decrease IBW by 10-15%, tetraplegia - by 1520%, respectively). The weight in admission is probably
the most reliable measure of weight in determining the actual body weight (ABW) of the patient because is unreliable
postoperatively or during an acute illness due to administra-tion of fluids or due to edematous condition. As a chronic
index, one can assume that the weight gain or loss is associated with an increase or decrease in lean body mass. To
determine the weight which should be used on the nutritional
calculations, first % IBW should be calculated through theequation: % IBW = actual body weight (actual body weight,
ABW / ideal body weight (IBW) x 100. If the actual bodyweight (ABW) is less than IBW, use ABW, to define the nutritional requirements, if is greater than IBW, but less than
120%, it is necessary to determine nutritional needs using
the adjusted relationship of body weight in the calculationneeds: IBW + (ABW - IBW x 0.25). The nutritional statusof patients can be categorized according to their ABW as apercentage of IBW as follows: over 200% of IBW (pathologic obesity), over 150% of IBW (obese), more than 120%
IBW (overweight), 100% of IBW +/- 10% (normal), 80-90%
of IBW (mildly malnourished), 70-80% of IBW (moderately
malnourished), less than 70% of IBW (severe nutritional
deficiency-malnutrition), respectively [3]. In generally anthropometric measures in spinal cord injured persons tend
to underestimate fat percentage when compared with ablebodied individuals.
Biochemical measurements
As with the visceral and somatic visceral proteins, non-dietaryfactors (i.e. blood loss, chronic infections, and fluid overload)
should be considered as potential reasons for the reductionof serum concentrations [3]. Proteins are essential for tissue
growth, maintenance and rebuilding their synthesis of hormones, enzymes, antibodies and cells transport molecules. If
excess protein or metabolized for energy or stored as fat. The
recommendations for protein intake in patients with spinal
cord injury vary with respect to acute or chronic phase of thelesion and the presence of decubitus ulcers or not.
Specific proteins (albumin, transferrin, and pre-albumin)
are biochemical indicators used for assessing nutritional status [23]. The level of serum albumin is not a definitive measure of visceral protein status, but reflects the complex relationship between synthesis, degradation, and distribution.

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J Clin Med Res • 2012;4(4):227-236

Given the long half-life of 21 days, serum albumin cannot beeffectively used for monitoring the acute response to nutritional therapy. Therefore, albumin levels should be includedin the initial profile for food control and monitoring purposes
during hospitalization for measuring trends of visceral protein or as an indicator of chronic nutritional status (Table 2).
Beside this limitation there are many non-dietary factors that
reduce the levels of albumin, regardless of nutritional status(inadequate composition: acute stress, hypoxia, impaired digestion, as in malabsorption, modified status as edematous
fluid status and fluid overload, chronic loss of protein).
Due to the lower half-life (8 - 9 days) and the smaller
size as a constituent body, transferrin is a better indicator of
nutritional status of visceral protein from albumin. Normal
levels of transferrin are between 200 - 400 mg/dl, and 150
mg/dl are considered nutritionally decision point or a point
where nutritional support should be revised or adjusted. The
transferrin levels are reduced in impaired synthesis as chronic
infections, increased secretion, fluid overload, increased ironstores and increased in reduced iron stores as iron deficiency
anemia and chronic blood loss, increased protein synthesis
on estrogen therapy and oral contraception and dehydration.
The serum concentration of transferrin is approximately 0.8
times the total iron binding capacity (TIBC). If direct measurement of transferrin is not possible due to the high costand limited availability of equipment required, the level oftransferrin can be easily calculated from TIBC, using the following formula: TIBC x 0.8 - 43 = transferrin [24].
The third protein biochemical indicator is pre-albumin,which has very short half-life (2 days), making it an excellent nutritional index and due to this reason is increasingly
used as an indicator of response to nutritional therapy. Reference values for pre-albumin are 16 - 35 mg/dl. A value of
dietary intervention is 11 mg/dl because a value below thislevel means malnutrition. The failure of patients to increasepre-albumin above 11 mg/dl with dietary therapy is an indication that nutritional needs are not met. Concentrations
should increase about 1 mg/dl per day or twice a week when
the treatment is the appropriate. Non-dietary factors that reduce pre-albumin include stress, inflammation [25-27].
Physical measurements include protein nitrogen balance studies and measurement of creatinine/height index(CHI). Nitrogen balance studies measure the net change intotal body protein. An assessment of nitrogen balance can beachieved by measurement of urinary urea (UUN) and compare it with the intake of nitrogen at the same time. The nitrogen balance is calculated as follows: N2 = balance intake
N2 - N2 elimination or = [protein (gr)] - (24 hour UUN + 3)
[6.25 gr nitrogen]. An “agent” of 3 is added to the equation
for nitrogen losses in feces, skin, and the drainage of body
fluids. When calculating the nitrogen balance a value of 0
meaning nitrogen balance (healthy adults), nitrogen balance> 0 (protein anabolism exceeds catabolism, usually consistent with pregnancy, growth, and recovery from disease or230

may indicate nutrient saturation, the goal in nutrition replenishment is a positive nitrogen balance of 4 - 6 grams per
day and nitrogen balance < 0 (the protein catabolism exceeds
protein anabolism, occurs in situations of famine, increased
catabolism due to trauma or surgery, and inadequate nutrition therapy), respectively. CHI measures the 24-hour creatinine excretion in urine and compares with an optimum value
based on the ideal weight for height [28].

Physiopathological Mechanisms of Malnutrition in Acute and Chronic Spinal Cord Injury
Energy expenditure in spinal cord injury
There is a dramatic increase in energy expenditure, endogenous protein catabolism and nitrogen excretion after injury.
Extensive multiple organ trauma, soft tissue injuries andfractures commonly associated with spinal cord injury, may
further increase hyper catabolic reactions. Also, after spinal
cord injury the body temperature and energy expenditure increases due to pulmonary infections or urinary tract infractions, and pancreatitis. The metabolic rate does not seemto be affected by the small reductions in thyroxin levels inplasma observed after the injury [29-31].
The energy requirements are evaluated in different ways.
To determine accurately the early energy expenditure after
spinal cord injury, studies compared measurements of real
resting energy expenditure (REE) with the Harris-Benedict
equation (basic energy expenditure, BEE) [18]. During thefirst two weeks after the injury, the exact measurements of
REE are similar to the estimated calorie needs, when usedwith BEE stressor/injury factor of 1.6. To avoid overestimation of calorie needs, the deletion of factor activity of 1.2(rest in bed) is proposed. Kearns et al. reported that in 10
patients, the mean REE after acute injury was only 67% of
BEE predicted by Harris-Benedict formula. They hypothesized that non-specific changes in neurogenic stimuli andreduced oxygen consumption by relaxing muscles contributed to their findings. Also, an interesting feature observedis that the REE was raised by 5% with the return of muscle
tone [32]. Jeejeboy and Cerra proposed an alternative approach that uses body weight (kg) alone as a determining
factor, and omits the variables of age, sex and height as usedin HB equation. This type of assessment has proven to beaccurate and efficient over time [33, 34]. Ireton-Jones andOwen et al. have developed specific formulas for the obese
patient, which is common in SCI subjects. The predefined
types may overestimate their needs due to increased fat massin this population [35, 36].
Nitrogen balance
Acute post-traumatic nitrogen requirements are much higher

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Malnutrition in Spinal Cord Injury
than in normal state. The accelerated catabolism of muscle
mass results in a supply of amino acids for the acute-phaseof protein synthesis, gluconeogenesis, and the healing ofwounds. Moreover, administration of glucocorticosteroids
after injury may increase the catabolism of protein. The
losses of nitrogen in the urine, mainly due to muscle atrophy
because of paralysis, are increasing with the severity of the
injury. On the other side, Cooper and Hoen stated that the secretion of more than 25 gr/day of nitrogen in the urine during
the first two weeks after the injury is insufficient prognostic
indicator for functional recovery of paralyzed muscles. The
nitrogen losses after an injury are always present and lastat least 7 weeks. In cases of acute injury, despite the provision of sufficient quantities of calories and protein usuallyoccurs a negative nitrogen balance (NB), which peaks during
the third week after injury. The same phenomenon has been
observed in cases of severe poisoning with botulinum toxin(botulism) which resulted in paralysis of muscles. Negative
nitrogen balance following injury, has been associated withfurther findings. During the first weeks after injury, many
patients experience a transient positive nitrogen balance,
possibly due to initial delays in the loss of nitrogen [37].
Four conscientious objectors were immobilized on pelvic
corset and leg casts for 6 to 7 weeks in a metabolic chamber.
All 4 subjects showed an increase in nitrogen excretion andnegative nitrogen balance. However, it took 4 to 5 days todevelop. In conclusion, acute immobilization of paralyzed
patients contributes to increased excretion of nitrogen whichstarts about a week after the injury [38].
Impaired glucose and lipid metabolism
Glucose and lipid metabolism disrupt in acute post-traumatic
phase. Increased hepatic gluconeogenesis and regional response to insulin result in hyperglycemia. The metabolism
of glucose in combination with acute nerve injury has beenstudied extensively, especially as related to ischemia. Thesestudies suggest that hyperglycemia which follows immediately after head injury or spinal cord may worsen the outcome. High serum glucose levels increase the availability of
substrate for anaerobic glycolysis, and thus the production oflactic acid, which may have the reverse effect on neurological recovery from injury. The prevention of hyperglycemia,
particularly during the first 2 to 8 hours after injury, seems tobe very critical for optimal recovery. After 2 to 8 hours after
injury, elevated glucose levels may be beneficial, allowing
the beginning of intestinal or parenteral feedings in a shorttime after the injury. It is also likely the serum triglyceride
levels to be found elevated due to the accelerated lipogenesis, decreased lipoprotein lipase activity, and impaired clearance of triglycerides [39].
Glucose is the preferred energy molecule for the central
nervous system, red blood cells, the cellular tissue, etc. A
minimum quantity of 100 - 150 gr glucose per day is required

J Clin Med Res • 2012;4(4):227-236
for these functions and prevents the consumption of endogenous protein. The normal rate at which the body metabolizes carbohydrates or glucose is approximately 2 - 4 mg/ Kg/
min. In times of severe stress, glucose metabolism may be
increased to 3 - 5 mg/Kg/min. In most patients, administration of more than 400 - 500 gr glucose per day, exceeding the
body’s ability to metabolize and stored as energy. Sources of
glucose include not only the liquid diet and peritoneal fluid
filtration. Excess glucose is converted into fat (lipogenesis)
and leads to an increased ratio of VCO2/VO2 (or RQ) [40].
The provision of lipids as a source of increased calories can facilitate protein maintenance, reduce the risk ofexcessive carbohydrates and reduce the total volume of liquid. Lipids are required to account for 30% of total calories supplied. In the acute phase after injury, large amountsof fat, especially as linoleic or omega-6 fatty acids have an
immunosuppressive effect by triggering the release of arachidonic acid. This leads to synthesis of prostaglandins andthen compresses the delayed hypersensitivity cell-regulated,
proliferation of lymphocytes. In the presence of sepsis, highlevels of serum triglycerides (250 gr/ml) indicate limited tolerance and decreased need for intravenous fluid delivery. A
minimum of 4% of total energy requirements is necessary
for the essential fatty acids to avoid deficiencies. Patientswith longstanding spinal cord injury are at increased risk for
cardiovascular disease and cardiopulmonary disease becauseof extensive fat intake and limiting activities. The reduced
intake of fats and cholesterol is a nutritional counseling intervention in this population to reduce the risks [41].
Deficiencies in zinc and vitamin C have been associatedwith poor wound healing. The provision of these micronutrients supplementation in patients with SCI with these deficits
enhances the healing. Adequate quantities of salts and vitamins are usually provided in a balanced diet. The supplemental micro-nutrient dietary substances are necessary if we suspect shortcomings intake or increased requirements becauseof circumstances specific diseases. Deficiencies of zinc, vitamin C, vitamin D have been associated with patients withspinal cord injury. Zinc is often prescribed to improve stressulcers, is known to be involved in structural integrity of collagen. However, zinc levels in serum is similar in patientstaking supplements that contain sulfur (220 mg daily) anddo not affect the healing process of ulcers sprawling over a
period of 2 - 3 months. Opposite physiological effects, suchas metabolism of copper, copper deficiency and anemia may
be caused by long-term supplementation of large amounts ofzinc [42]. The role of vitamin C in collagen synthesis is crucial. Although the supplementation with vitamin C did not
accelerate the healing of decubitus ulcers in patients, dietaryintake of vitamin C has not been associated with the development of decubitus ulcers. Moreover, given that the subclinical deficiencies are difficult to show up, the minimum
recommended dietary intake is proposed to 60mg [43].
Patients with spinal cord injury are prone to develop-

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J Clin Med Res • 2012;4(4):227-236

ing vitamin D deficiency. Earlier work by Bauman et alsuggested that approximately 32% of veterans with spinal
cord injury (SCI) were absolutely deficient in vitamin D(25 hydroxyvitamin D [25(OH)D]). Most subjects have ahigh incidence of vitamin D deficiency as defined by levels of 25(OH)D < 20 ng/mL. The reasons might be due to a
combination of low dietary vitamin D intake and avoiding
sun exposure because of depression or sensitivity in drugs
i.e. dantrolene. In the group of patients with spinal cord injury there was a negative correlation between serum levelsof 25-hydroxy-vitamin D and parathyroid hormone. Boneloss increases when there is secondary hyperparathyroidism
which complicates the osteoporosis in these patients. For thisreason, steps must be taken to correct these disorders [44].
Predisposing factors include also failure to sunlight due tohospitalizations and reduced mobility. There is a direct link
between sunlight exposure and vitamin D3 production in
the skin, which is biologically inactive but is converted by
25-hydroxylase (25-OHase) enzyme in the liver to 25-OH
D, the circulating form of vitamin D. The low intake of vitamin D, which is supplied by food either in vitamin D2 (ergocalciferol, activated ergosterol), found in yeast, or vitamin
D3 (cholecalciferol), found in fish, can be bypassed throughsupplements [45].

Discussion
Nutritional deficiency
The average daily dietary needs are modified because of thealtered physiology of each body system and psychologicalintegrity of a patient susceptible to an injury, potentially at
any age, which cannot exclude the possibility of a pre-existing disease causing nutritional problems [46]. Moreover,the frequent coexistence of spinal cord injury with injuries
from other systems, such as brain injury, maxillofacial injuries, fractures, etc., disturbs the normal physiology further.
Spinal shock is common after spinal cord injury, can persist
for weeks, and is leading to severe hypotension and further
complication such as fever, infections, sepsis, and the needfor surgery (which may exaggerate the use of body protein
for energy-gluconeogenesis) increasing the metabolic rate
[47-52]. Studies in malnourished patients stated that malnutrition before a spine stabilization surgery is leading topostoperative complications, hyperthermia, which increases
the caloric needs of the patient, and denervation, leading toatrophy and paralysis, which supply amino acids for gluconeogenesis, which, in turn, supplies glucose to meet caloric
needs [3]. Metabolic changes are also present with the elevated circulating levels of glucagon, cortisol, catecholamine and cytokines after injury to be primarily responsible
for the initial changes in metabolism. Glucose intolerance,
which cannot be readily apparent during the acute phase, but

232

may be caused by complications and physiological processesof acute care such as the initial hyper metabolic - catabolic
stress response, administration of steroids, the parenteral /enteral nutrition, and atrophy as a consequence of aponeurosis which results in gluconeogenesis [49]. Another serious
metabolic issue is negative nitrogen balance, due to excessive secretion of nitrogen because of protein use by the bodyto meet energy needs in the first week, with a peak at 3 weeks
and can last for a period of 7 weeks. This imbalance will respond only slightly increased protein intake and may be nonmodifiable as a process during the acute phase. The more
severe the injury the greater the amount of nitrogen excreted.
Excessive excretion of potassium and abnormal hyponatremia; hypercalcemia, due to immobilization, particularly inyoung men and hypercalciuria exceed the normal range in 4
weeks, with higher values at 16 weeks, which can persist fora long time. Hypercalcemia occurs with anorexia, abdominal
cramps, nausea, vomiting, constipation, polydipsia, polyuria,
dehydration and did not respond to diets which restrict the
intake of calcium and need to be treated with medication,
hydration, and mobilization [49, 53].
Obesity in spinal cord injury
Obesity in spinal cord injured subjects is mainly central orabdominal obesity leading to metabolic, cardiovascular issues etc. There is conflicting evidence about the contribution of visceral and subcutaneous adipose tissue to different
metabolic disorders after SCI. In the past anthropometricmeasures have been used for the prediction of adipose tissue’s distribution which now days have been replaced bymore sophisticated body composition technologies like dualenergy X-ray absorptiometry (DXA), highly precise quantitative techniques such as computerized tomography (CT)and magnetic resonance imaging (MRI) quantifying fat more
precise [54, 55]. In a chronic SCI population with paraplegia
values of body mass index (BMI, kg/m2) were not significant
vs. controls, which is a finding in line with the literature [9,56]. Nevertheless, Gupta et al demonstrated the usefulnessof BMI as an indicator of obesity, in body composition inpeople with spinal cord injury included both tetraplegics andmiddle-aged people unlike the Greek one which included
relatively young individuals [9, 57]. Whether the criteria of
BMI may assess obesity in people with spinal cord injury thelatest studies show the opposite [58]. In another study 50%
of SCI males were overweight by BMI, and more than 10%
were classified as obese. Overall, when compared with thegeneral population-observed distribution by BMI, a greater
proportion of men with SCI fell into the desirable BMI range
and fewer fell into the obese category [59]. These findings
show that using the BMI does not contribute substantiallyin determining the body composition of paraplegics andlowers the percentage of fat in this population, finding thatagrees with other studies and shows that the anthropometric

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Malnutrition in Spinal Cord Injury
measurement with BMI in paraplegics, underestimates fat inbody composition when measurements are compared withhealthy subjects [60]. Body mass index is a very simple measurement of fat; however it does not distinguish the individual components of weight. The applicability of conventional
BMI cut off values is into question [59, 61]. Another critical issue is that the relationship between BMI and disease istypically U- or J-shaped with those in the middle categories
of BMI having the lowest risk compared to the lowest extreme and upper levels of BMI. It is under question if the cutpoints for underweight, normal, overweight, and obese usedin able-bodied populations can be applied to SCI subjects.
If we choose percent body fat to measure obesity in SCI it
seems that SCI individuals may be at elevated risk; however,more studies are needed to define cut-off points of obesity in
SCI subjects and analyzing the impact injury types and duration of injury on the extent of obesity [62, 63].
Complications of spinal cord injury leading to malnutrition [64]Serum hemoglobin and hematocrit may reflect a generalstate of malnutrition. Anemia, defined by low hemoglobin
levels (< 14 mg/dl) and hematocrit (< 36%) reduces the oxygen in the blood and impedes the wound healing. Anemia
may be due to a preexisting condition or as the result of unbalanced production and distribution of blood cells as a result of reaction to stress, gastrointestinal bleeding or obvious
bleeding due to other trauma [65]. Low levels of total serum
protein (< 6.4 mg/dl) and protein (< 3.5 mg/dl), accelerate
the development of edema, which causes a decrease in skinelasticity and prevent the transfer of oxygen and nutrientsfrom the blood to the skin. Also, the swelling may increase
local tissue pressure, causing loss of regional blood flow andtissue damage. The loss of protein and protein secretion inpressure ulcers increases the deficiencies in proteins. Moreover, reduced mobility and immobilization for long periodcause pressure ulcers of the skin and the wound but can beprevented by adequate intake of quantity of protein, vitaminE, zinc, and fluids to maintain skin integrity [66].
Pneumonia and paralysis of respiratory muscles throughmalnutrition may further weaken the respiratory muscles.
On the other site excessive feeding may lead to increasedoxidation of glucose and production of carbon dioxide to beeliminated and further stress on the respiratory system. The
fluid overload or aggressive implementation of parenteralsupport can lead to pulmonary edema. The reduced hydration can lead to reduced drainage of secretions, atelectasis,and pneumonia. Abdominal distension due to unabsorbed
food by mouth or enteral feeding or swallowing air during feeding can lead to compromise the functioning of thediaphragm and predisposes to hypoventilation or aspiration[67]. The paralytic ileus occurs as a result of disturbance of
the autonomic and simultaneous or ischemia as a complica-

J Clin Med Res • 2012;4(4):227-236
tion of hypokalemia, abdominal trauma or sepsis, generally
persists for 72 hours - 1 week and may restrict the movementof the diaphragm [68]. Parenteral nutrition is indicated if
persists for more than 3 - 5 days. Ulcers and bleeding, which
occur as a result of paralytic vasodilatation with ischemia,
steroids, nasogastric tube irritation, and other causes shouldbe treated with oral or enteral feeding as soon as possible but
may require parenteral nutrition [69]. Neurogenic bowel requires the right amount of food, fiber and fluids in order to be
successful retraining of the bowel, and prevent constipation,
diarrhea, incontinence, and autonomic dysreflexia as a resultof fecal impaction. Bowel function may be compromised byhyperosmolar feeding through a tube, lactose intolerance or
pseudomembranous colitis, prolonged treatment with antibiotics, which can cause diarrhea and require parenteral nutritional support. For neurogenic bladder vitamin C and othersupplements are necessary for the acidification of urine andprevention of infection of the urinary tract. The inability of
individuals with spinal cord to receive adequate food supply,
may be caused by anorexia, early satiety, dysgeusia, smellingproblems, immobility, depression, and swallowing disorderi.e. dysphagia or silent aspiration, (caused by a cervical spine
stabilization vest like Halo type or other restrictive devices,
i.e. a tracheotomy tube, and injuries or nerve palsies and requires parenteral or enteral support, as soon as possible toprevent pressure ulcers), cause anemia and gastrointestinal
complications such as stress ulcers, pancreatitis, and reduced
mobility. Finally the effect of drugs such as analgesics andbarbiturates is crucial.
Financial
No benefits in any form have been received or will be received from a commercial party related directly or indirectly
to the subject of this article.

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