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Benton B, Iruthayarajah J, Longval M, McIntyre A, Blackport D, Muise S, Teasell R. (2019). Nutrition Issues Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Noonan VK, Loh E, Sproule S, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence. Version 7.0: p 1-69.
The nutritional aspect following a spinal cord injury (SCI), is a complex and multifactorial challenge. SCIs can cause devastating short and long-term impairments in physical, cognitive, and psychological status. Specifically, post-SCI cognitive and oropharyngeal impairment may result in decreased tongue movement while chewing and reduced pharyngeal movement, all which ultimately delay the passage of food to the esophagus.
Resting metabolic rate, physical activity and the thermic effect of food are all factors that contribute to energy expenditure and a healthy weight, which can be challenging for patients to achieve and maintain post-SCI. The resting metabolic rate of people with chronic SCI is estimated to be 14-27% lower than their non-SCI counterparts, largely due to reductions in fat-free mass and reduced sympathetic nervous system activity. Physical activity levels of persons with SCI are also generally lower than that of non-SCI persons. Finally, individuals post-SCI can have substantial limitations to their mobility, and thus caregivers may play a large role in meal planning and diet adherence.
In persons with SCI, the usual clinical measures of total body fat, such as weight and body mass index (BMI), underestimate the degree of adiposity. The metabolic alterations related to adverse body composition changes, decreased physical activity and other factors in individuals with SCI are considered atherogenic.
Alterations in the central or peripheral nervous system can result in delayed gastric emptying, prolongation of intestinal transit time, and poor colonic motility, collectively known as neurogenic bowel. Neurogenic bowel has a significant impact on the quality of life of individuals with SCI, contributing to morbidity and even death. Pressure ulcers are common following SCI, and healing can be compromised by suboptimal nutrition status. After a SCI, patients with pressure ulcers have lower zinc, albumin and prealbumin levels than those without pressure ulcers. Impaired nutritional status contributes to delayed or incomplete wound healing. Osteoporosis is common in SCI and results in increased bone fragility and fracture risk (Warden et al. 2001). In addition to pharmacological and other management strategies, supplementation with nutrients such as calcium and vitamin D may play a role in bone health following SCI.
Individuals after SCI commonly experience chronic inflammation, which is associated with immune impairment which can lead to infections and other dysfunctions. Cardiovascular disease appears prematurely in persons with SCI. It is the most frequent cause of death among persons surviving more than 30 years following injury and accounts for 45% of all SCI deaths.
Although little work has been done examining the vitamin profiles of individuals following SCI, it is generally thought that vitamin deficiency is a significant issue. Studies have shown that 16% to 37% of community-dwelling SCI subjects had serum levels below the reference range for vitamins A, C, D and E compared with general population norms. Vitamin D deficiency promotes calcium deficiency and secondary hyperparathyroidism, resulting in further bone loss and exacerbating osteoporosis. Myopathy and nonspecific musculoskeletal pain may also develop as a consequence of vitamin D deficiency. Vitamin B12 deficiency in persons with SCI is reported to be between 5.7% and 19%, with symptoms may include declining gait, depression or fatigue, upper limb weakness, memory loss and worsening pain.
There is a scarcity of intervention studies investigating nutritional status and associated risk for persons with SCI, and more research is needed in this field.
|Gaps in the Evidence|