Users Online: 2154

Home Print this page Email this page Small font sizeDefault font sizeIncrease font size

Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 

   Table of Contents      
Year : 2019  |  Volume : 9  |  Issue : 3  |  Page : 111-115

Medical Nutrition Therapy for a Critically Ill Patient With Spinal Cord Injury: A Case Report

1 Department of Nutrition, Faculty of Medicine, Universitas Indonesia, Cipto Mangunkusumo Hospital, Jakarta, Indonesia
2 Department of Orthopaedic and Traumatology, Faculty of Medicine, Universitas Indonesia, Cipto Mangunkusumo Hospital, Jakarta, Indonesia

Date of Submission18-Mar-2019
Date of Decision22-Apr-2019
Date of Acceptance29-May-2019
Date of Web Publication25-Oct-2019

Correspondence Address:
Ahmad Jabir Rahyussalim
Faculty of Medicine, Department of Orthopaedic and Traumatolgy, Universitas Indonesia, Jalan Salemba 6, Kelurahan Kenari, Kecamatan Senen, Jakarta Pusat, DKI Jakarta, 10320
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijnpnd.ijnpnd_13_19

Rights and Permissions

Spinal cord injury causing chronic paralysis affects the body’s energy and protein requirements. Central nervous system injuries require long-term healing, and its complications can lead to prolonged bed rest, decreased life expectancy, and reduced quality of life. The risk of malnutrition due to chronic inactivity can lead to a loss of muscle mass, which affects nutritional status. Medical nutrition therapy aims to decrease the metabolic response, maintain fat-free mass, and prevent complications. We report a 58-year-old critically ill man with a spinal cord injury who had a normal weight initially; his medical nutrition therapy was based on nutrition guidelines for critically ill patients and gradually increased as per his clinical and gastrointestinal tolerance. He was given vitamin B supplementation and treated for 69 days. On discharge, he had optimal oral nutrient intake and normal weight. Adequate nutrition supported his recovery, increased his functional capacity, and maintained his nutritional status.

Keywords: Critically ill, medical nutrition therapy, spinal cord injury

How to cite this article:
Krisadelfa S, Inge P, Diana S, Johana T, Rahyussalim AJ. Medical Nutrition Therapy for a Critically Ill Patient With Spinal Cord Injury: A Case Report. Int J Nutr Pharmacol Neurol Dis 2019;9:111-5

How to cite this URL:
Krisadelfa S, Inge P, Diana S, Johana T, Rahyussalim AJ. Medical Nutrition Therapy for a Critically Ill Patient With Spinal Cord Injury: A Case Report. Int J Nutr Pharmacol Neurol Dis [serial online] 2019 [cited 2022 Oct 4];9:111-5. Available from:

   Introduction Top

Spinal cord injury can lead to sensory, motor, and autonomic disruptions that affect physical, psychological, and social life.[1] The risk of mortality in the first year after the injury is approximately two to five times higher than in individuals who have no injury.[2] Long-term complications reduce life expectancy and quality of life.[1],[3],[4],[5],[6] Research on nutritional medical therapy in patients with spinal cord injury is still limited; hence, there is no established guideline for conducting standard medical nutrition therapy for those patients. Thus, for our patient, medical nutrition therapy was implemented in accordance with the recommended nutrition guidelines for critically ill patients, as provided by the American Society for Parenteral and Enteral Nutrition-Society of Critical Care Medicine (ASPEN-SCCM) in 2016.[7]

   Case History Top

A 58-year-old man had a decrease in consciousness due to a traffic accident 8 h before admission to the hospital. He had no nausea, vomiting, or seizures. Upon arrival at the Emergency Room of Cipto Mangunkusumo Hospital, the patient was resuscitated and a series of X-rays was taken. The doctor decided to stabilize his right upper extremity and left lower extremity with surgery.

There was no medical history of decreased body weight (BW) or other illnesses. The patient smoked about two packs (20 cigarettes) per day and drank five cups of brewed coffee per day. Within 24 h, the patient received 1010 kcal (17 kcal/kg BW). Liquid food was provided enterally (via nasogastric tube, NGT) in quantities of 2 × 50 mL and improved to 13 × 70 mL.

The first and second day of hospitalization, the patient did a series of surgeries. A few hours after surgery in the second day of hospitalization, the patient received clear fluid 30 mL/h because he had a 550 mL residue from NGT within 24 h. The patient got in the form of liquid food from the hospital and commercial high-protein liquid food through the NGT in the third day of hospitalization when the residue was only 50 mL in the third day and no residue in the next days.

A clinical nutrition assessment was performed on the third day. The patient had an inadequate contact and used mechanical ventilation with midazolam 1 mg as sedation. From anthropometric measurements we obtained an estimated BW of 60 kg [upper arm circumference (UAC) 22.5 cm], body length 170 cm, and body mass index (BMI) 20.7 kg/m2, which categorized as normoweight, based on the criteria of the World Health Organization (WHO) Asia Pacific.

On physical examination, the patient had a Glasgow Coma Scale score of E4M0V0 with dopamine 10 mcg as a vasopressor. His blood pressure (BP) was maintained at 162/74 mmHg with mean arterial pressure 110 (82–112) using dopamine; his pulse was 69 times/min, temperature 36°C, respiratory rate 14 per minute with synchronized intermittent mandatory ventilation mode 9, positive end-expiratory pressure +5, fraction of inspired oxygen 40%, and oxygen saturation (O2) 98%. The patient’s BP on admission was 70/50 mmHg with a pulse 51 times/min. His conjunctiva appeared anemic, and a NGT was inserted that only produced a 50-mL milky white residue within 24 h. We placed a neck collar and a central venous catheter. The results of the examination of his heart, lungs, and abdomen were within normal limits. His right arm was fixated with a long cast and a backslab was attached to the left leg. His functional capacity was bedridden.

The neurological examination revealed 3 mm/3 mm isocor round pupils, there were no abnormalities of the cranial nerves, and sensory and autonomic functions were not assessed. There was an impression of upper motor neuron tetraparesis, with upper motor strength [American Spinal Injury Association (ASIA) Classification]: 1xx1 | 3431, lower motor strength: 1000 | xxxx, physiological reflex of the upper extremity: x | +2, lower extremity: +2 | x, negative bilateral pathological reflexes.

Laboratory data revealed anemia with hemoglobin levels 8.4 g/dL; leukocytosis 16.000/µL, hyperkalemia 5.8 mEq/L, hypoalbuminemia 2.9 g/dL, elevated serum glutamic oxaloacetic transaminase 74 IU/L, serum glutamic pyruvic transaminase 81 IU/L, and blood gas analysis showed metabolic alkalosis.

The patient was diagnosed as normoweight with a risk of malnutrition, severe hypermetabolism, and retrolisthesis at vertebrae cervical 5–6 (C5–C6) with spinal shock and neurogenic shock. Debridement and external fixation were indicated for a left fibular tibial fracture and closed reduction was indicated for the right ulnar radius fracture. The nutrition therapy prescribed was 1230 kcal (21 kcal/kg BW), protein 56.5 g (0.9 g/kg, 18%, N: NPC ratio; nitrogen: noncalorie protein ratio = 1:111), fat 31 g (23%), and carbohydrate 187 g (59%) in the form of liquid food from the hospital and commercial high-protein liquid food through the NGT. The nutrition was administered in five cycles, and each cycle consisted of 3 h administration of liquid and 1 h of rest, starting at 70 mL/h and increasing to 90 mL/h. The patient also received micronutrient vitamin B supplementation during treatment in hospital, in the form of vitamin B6 (2 × 10 mg) and B12 (2 × 50 mg) given via NGT. The therapy gradually increased up to 30 kcal/kg in accordance with clinical and gastrointestinal tolerance. The patient reached 30 kcal/kg on the 29th day of treatment.

The patient was treated for 69 days, with treatment in the ICU for 32 days, then in the high care unit, and was finally moved to the usual care ward. On the third day of monitoring, the patient had been extubated, but still had a titrated vasopressor. However, on the sixth day, the patient was desaturated and returned on the ventilator, and the vasopressor dose was increased. On that day, the patient was remeasured anthropometrically, and the UAC was 21 cm (a decrease of 1.5 cm from the initial measurement). At that time, protein intake only reached 1.1 g/kg BW, so nutritional assessment focused on increasing protein up to 1.6 g/kg BW. The patient was extubated on the 21st day of treatment. From the 21st until the 34th day of treatment, the patient was able to breathe spontaneously with oxygen, and we planned to step-down to high care unit. On the 45th day of treatment, the vasopressor was removed and the patient was transferred to the usual care ward. At that time, the patient was remeasured anthropometrically, and the UAC was 20 cm (a decrease of 1 cm from previous measurement). The patient experienced clinical improvement, and at the end of treatment, his upper motor strength as measured by the ASIA Classification was: 1xx3 | 3431, lower motor strength: 2000 | xxxx, sensory: hypesthesia as high as C5, autonomic functions demonstrated urinary incontinence and alvi, physiological reflexes of the arm: x | +2, leg: +2 | x, negative bilateral pathological reflexes.

At the end of his treatment he had no dysphagia by swallowing test confirmation, so he had been got parenteral nutrition. He had reached 1850 kcal (34 kcal/kg), protein intake 78 g (1.4 g/kg), with protein fulfillment target up to 1.6 g/kg, fat 41 g (20%), carbohydrate 270 g (63%) in the form of 1100 kcal porridge, 2 × 250 mL commercial high-protein liquid food, and 1 × 250 mL liquid food from the hospital.

   Discussion Top

The patient’s motor strength was measured by assessing dermatomes and myotomes according to the ASIA Classification. He had upper motor strength: 1xx1 | 3431 and lower motor strength: 1000 | xxxx. On the 45th day of treatment, the patient was reexamined for his motoric strength, and the results were upper motor strength: 1xx3 | 3431 and lower motor strength: 2000 | xxxx.

The exact mechanisms underlying motor repair after spinal injury are still unclear, but it might be related to the role of glycogen synthase kinase-3β (GSK-3β). This enzyme plays a role in the inhibition of glycogen synthase, which influences growth and development and inhibits cell apoptosis. Research conducted by Cuzzocrea et al.[8] showed that patients who underwent laminectomy had edema and myelin loss in dorsal and ventral funiculi, which caused impaired motor function. This mechanism is inhibited by GSK-3β activity. Therefore, inhibiton of this enzyme is considered to be one of the therapeutic modalities that can improve the motor function of the spinal cord.[9] Beurel et al.[10] stated that negative regulation of GSK3 can also be mediated by phosphoinositide 3-kinase (PI3K)/Akt-mediated phosphorylation. One of the potent agent of PI3K/Akt is branched-chain amino acid (BCAA). Thus, administration nutrient containing BCAA could indirectly inhibit GSK3 activity. Another study conducted by Wu et al.[11] showed that giving vitamin B6 also increased P13K activity.[11] The patient also received vitamin B6 supplementation 2 × 10 mg. Therefore, nutritional factors can help improve motor function.

Cervical spine injury can result in complications such as neurogenic shock. In this case report, our patient also experienced neurogenic complications, with a history of BP and pulse of 70/50 mmHg and 51 times/min, respectively, during the first admission. Neurogenic shock occurs when the injury interferes with sympathetic innervation to the heart, and at the same time there is loss of vasomotor tone. Hypotension and bradycardia are classic markers of this type of shock.[9] Sympathetic innervation to the heart is innervated from thoracal 1 to 5 (T1–T5), thus, neurogenic shock can only occur if the injury is above the T6.[5] This patient had an injury above the T6 level at the C5–C6 level.

Critically ill patients often experience a delay in gastric emptying. Gastric motility can be influenced by several factors, such as hemodynamic instability, hyperglycemia, an electrolyte imbalance, hypoxia, sepsis, increased intracranial pressure, and the administration of a hyperosmolar formula. Gastric residual volume (GRV) assessment in critically ill patients is used to assess tolerance through the enteral route and the risk of aspiration pneumonia.[7],[12] However, GRV assessment is not routine for monitoring enteral tolerance of patients in the ICU. On the third day of hospitalization, there was substantial NGT residue, reaching 550 mL in 24 h with a whitish color. At that time, the hemodynamics of the patient, who was still unstable, were thought to be the cause of the high GRV. The cervical fracture also leads the patient to be unable to raise his head 30° to 45° when receiving fluids. This is also one of the causes of GRV.[13] Miller et al.[14] stated that hemodynamic instability and vasopressor requirements can increase the risk of gastrointestinal ischemia. Furthermore, Krejci et al.[15] added that the use of vasopressors causes decreased mesenteric blood flow.

Blood analyses revealed that the patient had anemia with a hemoglobin level 9.3 g/dL, which decreased to 9.16 g/dL on the third day of monitoring, and it further decreased to 8.4 g/dL on the sixth day of monitoring. Anemia in critical illness is caused by two main factors: the shortened life span of red blood cells and decreased red blood cell production.[16] Hypoalbuminemia also occurred in this patient, with albumin levels of 2.9 g/dL. Hypoalbuminemia is a prognostic marker for patients with spinal cord injury that reflects proinflammatory conditions and neurological deficits, axonal damage, and degeneration.[17] The patient had elevated serum transaminase levels, with serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase levels of 74 and 81 IU/L, respectively. The cause of increased serum transaminase levels in patients with spinal cord injury is not yet fully understood. Animal studies have shown an increase in the level of these enzymes in spinal cord injury as a result of macrophage activation and lipid accumulation due to cytokines. More than 70% of cases of spinal cord injury experience changes in liver function in the form of fat infiltration into the liver parenchyma.[18]

Critically ill patients are at risk of gastric ulcers. The American Society of Health-System Pharmacists recommends the prophylactic use of proton pump inhibitors (PPIs) or histamine-2 receptor antagonists as standard of care for patients at risk of gastrointestinal bleeding.[19],[20] The patient received prophylaxis in the form of PPI drugs and histamine-2 receptor antagonists for 5 days in accordance with American Society of Health-System Pharmacists recommendations. PPIs decrease food absorption by disrupting hydrogen adenosine triphosphate enzyme on the surface of parietal gastric cells, thus leading to vitamin B12 deficiency.[21] Therefore, the patient was administered vitamin B12 supplementation.

Enteral nutrition also reduces the risk of gastric ulcers because nutrients are buffers of gastric acid, increase mucosal blood flow, and induce mucus secretion.[21] The patient received early enteral nutrition (<24 h after admission), which is another preventive measure against gastric ulcers.

The nutritional status of the patient was measured by UAC. He experienced a 2.5 cm decrease in UAC during hospital treatment. Measurements of his anthropometric status were conducted by UAC because the patient was bedridden and had paresis. Bedscale was not available on the ward so the determination of the patient’s weight used the estimated body weight of the UAC. Some researchers have compared the correlation between BMI and UAC in determining the risk of malnutrition. BMI is said to be underestimated in patients at risk of malnutrition, especially in patients who experience fluid or ascites retention, whereas UAC offers better indicators for evaluation nutritional status.[22]

After the patient was moved to the usual care ward, the patient’s nutritional intake at the end of treatment had reached 30 kcal/kg. For patient with spinal cord injury, additional energy intake not only supplies necessary energy, but also spares protein reserves, primarily muscle tissue. Adequate protein is needed to prevent a negative nitrogen balance and reductions in immunocompetence, improve hypoalbuminemia, and accelerate wound healing.

The fulfillment of the minimum requirements of carbohydrate for the patient during treatment was 1.9 to 4.5 g/kg or 54% to 63% of the total energy requirement, which is in accordance with the ASPEN-SCCM’s recommendations. The adequacy of carbohydrate is important for the brain and for glucose-dependent red blood cells. Hyperglycemia is also a frequent problem in critically ill patients. The release of stress hormones causes a condition called stress-related insulin resistance and leads to hyperglycemia.[23]

Another mechanism that can explain the occurrence of hyperglycemia in patients with spinal cord injury is microglia activation. Okada[24] stated that overexpression of nuclear factor kappa B (NF-κB) in microglia cells causes hyperglycemia. This condition leads to an inhibition of the neuronal cell apoptosis process and increased demyelination, which worsens clinical output.[24] During hospitalization, the patient did not experience reactive hyperglycemia.

Adequacy of protein intake in critically ill patients is important for wound healing process and increasing acute-phase proteins in the context of inflammation. Protein intake and N:NPC ratio were achieved at 0.6 to 1.4 g/kg BW or 17% of the total energy requirement, with N:NPC = 1:101–127. ASPEN-SCCM recommends that protein intake reaches 1.2 to 2 g/kg/day with a minimum NPC ratio 1:70–100 to prevent a protein-sparing effect.[7],[25] The patient had elevated serum transaminase, which disrupted protein metabolism regulation. On the other hand, the patient also had hypoalbuminemia, which required a high protein intake. Therefore, protein should be given in the form of BCAA because this type of protein is not all metabolized in the liver and is partly metabolized in the muscle.[26] Food sources of BCAA include chicken, beef, cheese, and eggs. Approximately, 10 to 14 g/day of BCAA is needed, with a ratio of leucine:isoleucine:valine at 2:1:1.[27]

Fat intake is recommended by the European Society for Clinical Nutrition and Metabolism (ESPEN) to be 20% to 30% of total calories. The percentage of fat intake in our patient was 17% to 29%. The composition of fat in patients with spinal cord injury is expected to be balanced, not exceeding 30% of the total energy requirement, because these patients are at risk of postinjury obesity and cardiovascular disease.[28]

Micronutrients are needed in spinal cord injury cases for nerve cell regeneration. During his treatment in the ICU, the patient received micronutrients from high-protein commercial formulas. The patient also received vitamin B6 (2 × 10 mg) and B12 (2 × 50 mg) supplementation. Vitamin B helps to maintain neuron function by increasing production of Schwann cells and enhancing the myelinization of nerve cells,[29] and vitamin B6 and B12 counter neuron ischemia.[30] Administration of these vitamins in high doses is beneficial for decreasing axonal degeneration and improving muscle action potential recovery.[31],[32]

The functional capacity of the patient was assessed by spinal cord independence measures (SCIM).[32] The patient had a zero SCIM score, when assessed by mechanical ventilation. At the end of treatment, the patient’s respiration score was five, which indicated that he did not require the help of an endotracheal tube, but he did require oxygen assistance.SCIM consists of several parameters, namely how patient eats, baths, and dresses, cares for himself, spontaneous breathing, toilet management, gastrointestinal management, and mobility. The parameter that can only be assessed in patient is the assessment of respiration, because the others parameters are zero, which means the patient is totally dependent.

There is a risk of dysphagia in patients with spinal cord injury. Patients with an injury around the cervical area are at greater risk for dysphagia than those who have injuries at the lower cervical level.[33],[34] The patient in this case report did not experience dysphagia during a swallowing test, and he was discharged with oral nutritional intake.

After discharge from the hospital, the patient was advised to consume foods high in vitamins and minerals, such as vitamin C and zinc, from specific food sources. These food sources include fruits such as guava, papaya, pineapple, avocados, spinach, carrot, broccoli, and bananas. Vitamin C is useful for collagen synthesis, immunomodulation, and antioxidants, and deficiencies in this vitamin lead to an impaired immune response and decreased collagen synthesis. Zinc is a cofactor of polymerization of ribonucleic acid and deoxyribonucleic acid; thus, it plays a role in deoxyribonucleic acid synthesis, protein and cell proliferation, and collagen synthesis.[35],[36]

A study by Goodwin-Wilson et al.[37] showed that the prognosis of spinal cord injury is related to the patient’s age and the presence of autonomic disorders. At an age of ≥65 years, the presence of autonomic disorders such as urinary incontinence and gastrointestinal and reproductive system disorders are markers of a poor prognosis.[37] Although the patient was 58 years old, he had autonomic disorders. Nevertheless, his nutrition intake during treatment reached the target and he was able to consume food orally.

   Conclusions Top

Adequate nutrition for a patient with spinal cord injury supported his recovery, increased his functional capacity, and maintained his nutritional status. Increased protein requirement is needed because patient with spinal cord injury is often found to have hypoalbuminemia. However, choosing the type of protein must also be considered because the patient had elevated serum transaminase. BCAA is considered to be good choice because this type of protein is not metabolized in the liver, but is partly metabolized in the muscle. Adequacy of fat should not exceed 30% due to the risk of cardiovascular disease and obesity postinjury. Micronutrient vitamin B is needed for the recovery of nerve cells; in addition, vitamin C and zinc are also needed for immunity and wound healing.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Singh A, Tetreault L, Kalsi-Ryan S, Nouri A, Fehlings MG. Global prevalence and incidence of traumatic spinal cord injury. Clin Epid 2014;4:309-31.  Back to cited text no. 1
WHO 2013. Spinal cord injury. Available at [Accessed on 1st of May 2018; 20.36 pm].  Back to cited text no. 2
Gundogdu I, Ozturk EA, Umay E, Karaahmet OZ, Unlu E, Cakci A. Implementation of a respiratory rehabilitation protocol: weaning from the ventilator and tracheostomy in difficult-to-wean patients with spinal cord injury. Disabil Rehabil 2016;5:1-9.  Back to cited text no. 3
Berlly M, Shem K. Respiratory management during the first five days after spinal cord injury. J Spinal Cord Med 2007;30:309-18.  Back to cited text no. 4
Hagen EM, Faerestrand S, Hoff JM, Rekand T, Gronning M. Cardiovascular and urological dysfunction in spinal cord injury. Acta Neurol Scand Suppl 2011;124:71-8.  Back to cited text no. 5
Dakson A, Brandman D, Thibault-Halman G, Christie SD. Optimization of the mean arterial pressure and timing of surgical decompression in traumatic spinal cord injury: a retrospective study. Spinal Cord 2017;3:1-6.  Back to cited text no. 6
McClave SA, Taylor BE, Martindale RG, Warren MM, Johnson DR, Braunschweig C et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). J Parenter Enter Nutr 2016;40:159-211.  Back to cited text no. 7
Cuzzocrea S, Genovese T, Mazzon E, Cirsafulli C, Paola RD, Muia C et al. Glycogen synthase kinase-3β inhibition reduces secondary damage in experimental spinal cord trauma. J Pharm Sci 2006;12:79-89.  Back to cited text no. 8
Boswell K, Menaker J. An update on spinal cord injury: epidemiology, diagnosis, and treatment for the emergency physician. Trauma Rep 2013;14:1-9.  Back to cited text no. 9
Beurel E, Grieco SF, Jope RS. Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases. Pharmacol Ther 2015;148:114-31.  Back to cited text no. 10
Wu Y, Liu Y, Han Y, Cui B, Mi Q, Huang Y et al. Pyridoxine increases nitric oxide biosynthesis in human platelets. Int J Vitam Nutr Res 2009;79:95-103.  Back to cited text no. 11
Landzinski J, Kiser TH, Fish DN, Wischmeyer PE, MacLaren R. Gastric motility function in critically ill patients tolerant vs intolerant to gastric nutrition. J Parenter Enteral Nutr 2008;32:45-50.  Back to cited text no. 12
Boullata JI, Carney LN, Guenter P, American Society for Parenteral and Enteral Nutrition. A.S.P.E.N. Enteral Nutrition Handbook. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2010.  Back to cited text no. 13
Miller KR, Kiraly LN, Lowen CC, Martindale RG, McClave SA. Can we feed? A mnemonic to merge nutrition and intensive care assessment of the critically ill patient. J Parenter Enteral Nutr 2011;35:643-59.  Back to cited text no. 14
Krejci V, Hiltebrand LB, Sigurdsson GH. Effects of epinephrine, norepinephrine, and phenylephrine on microcirculatory blood flow in the gastrointestinal tract in sepsis. Crit Care Med 2006;34:1456-63.  Back to cited text no. 15
Rodriguez RM, Corwin HL, Gettinger A, Corwin MJ, Gubler D, Pearl RG. Nutritional deficiencies and blunted erythropoietin response as causes of the anemia of critical illness. J Crit Care 2001;16:36-41.  Back to cited text no. 16
Chao ZY, Deng SX, Zhou Y, Cao TW. Serum albumin is a predictor for duration of weaning in patients with traumatic brain injury. Int J Clin Exp Med 2016;9:4041-6.  Back to cited text no. 17
Trauner M, Arrese M, Wagner M. Fatty liver and lipotoxicity. Biochim Biophys Acta 2010;1801:299-310.  Back to cited text no. 18
ASHP therapeutic guidelines on stress ulcer prophylaxis. Am J Health Syst Pharm 1999;56:347-79.  Back to cited text no. 19
Plummer MP, Blaser AR, Deane AM. Stress ulceration: prevalence, pathology and association with adverse outcomes. Crit Care 2014;18:213-9.  Back to cited text no. 20
Heidelbaugh JJ. Proton pump inhibitors and risks of mineral deficiency: evidence and clinical implications. Ther Adv Drug Saf 2013;5:15-20.  Back to cited text no. 21
Brito NB, Lianos JBS, Ferrer MF, Garcia JGO, Brito ID, Castro FPG et al. Relationship between mid-upper arm circumference and body mass index in inpatients. Plos One 2016;11:e0160480.  Back to cited text no. 22
Nielsen ST, Krogh-Madsen R, Moller K. Glucose metabolism in critically ill patients: are incretins an important player? J Intensive Care Med 2015;30:201-8.  Back to cited text no. 23
Okada S. The pathophysiological role of acute inflammation after spinal cord injury. Inflamm Regen 2016;36:20-7.  Back to cited text no. 24
Stroud M. Protein and the critically ill: do we know what to give? Proc Nutr Soc 2007;66:378-83.  Back to cited text no. 25
Charlton M. Branched-chain amino acid enriched supplements as therapy for liver disease. J Nutr 2006;136:S295-8.  Back to cited text no. 26
Kurpad AV, Regan MM, Raj T, Gnanou JV. Branched-chain amino acid requirements in healthy adult. J Nutr 2006;136:256-63.  Back to cited text no. 27
Perret C, Stoffel-Kurt N. Comparison of nutritional intake between individuals with acute and chronic spinal cord injury. J Spinal Cord Med 2011;34:569-75.  Back to cited text no. 28
Altun I, Kurutas EB. Vitamin B complex and vitamin B12 levels after peripheral nerve injury. Neural Regen Res 2016;11:842-5.  Back to cited text no. 29
[PUBMED]  [Full text]  
Maladkar M, Tekchandani C, Dave U. Post-marketing surveillance of fixed dose combination of methylcobalamine, alpha lipoic acid, folic acid, biotin, benfotiamine and vitamin B6-nutripathy for the management of peripheral neuropathy. J Diabetes Mellitus 2014;4:124-32.  Back to cited text no. 30
Chen CH, Huang YK, Jaw FS. Ultrasound-guided perineural vitamin B12 injection for peripheral neuropathy. J Med Ultrasound 2015;23:104-6.  Back to cited text no. 31
Anderson K, Aito S, Atkins M, Sorensen FB, Charlifue S, Curt A et al. From the 2006 NIDRR SCI measures meeting functional recovery measures for spinal cord injury: an evidence-based review for clinical practice and research. J Spinal Cord Med 2008;1:133-44.  Back to cited text no. 32
Chaw E, Shem K, Castillo K, Wong SL, Chang J. Dysphagia and associated respiratory considerations in cervical spinal cord injury. Spinal Cord Inj Rehab 2012;18:291-9.  Back to cited text no. 33
Valenzano TJ, Waito AA, Stelle CM. Characterizing dysphagia and swallowing intervention in the traumatic spinal injury population. Dysphagia 2016;31:598-609.  Back to cited text no. 34
Quain AM, Khardori NM. Nutrition in wound care management: a comprehensive overview. Wounds 2015;27:327-35.  Back to cited text no. 35
Stechmiller JK. Understanding the role of nutrition and wound healing. Nutr Clin Pract 2010;25:61-8.  Back to cited text no. 36
Goodwin-Wilson C, Watkins M, Gardner-Elahi C. Developing evidence-based process maps for spinal cord injury rehabilitation. Spinal Cord 2010;48;122-7.  Back to cited text no. 37


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
   Case History

 Article Access Statistics
    PDF Downloaded175    
    Comments [Add]    

Recommend this journal