Traumatic SCI is one of several neurological disorders leading to disuse osteoporosis and resultant fractures, but it differs from many other clinical conditions in the rate of osteoporosis development. Approximately two weeks after acute spinal cord injury, a rapid process of bone resorption exceeding that of bone formation begins to occur, primarily due to upregulation of the osteoclasts [4, 5]. Given its faster turnover rate [6, 7], trabecular bone is more commonly affected than cortical bone in the first four months following SCI. During the first six months following acute SCI, markers of bone formation range from mildly depressed to slightly elevated, depending on the study cited [5, 8, 9]. Even if markers of formation are slightly increased, this compensatory process is not sufficient to counteract the significant bone resorption that occurs concurrently. Roberts and colleagues [9] observed a rapid rise in urinary values of total and free deoxypyridinoline, total pyridinoline, and NTX in the immediate period following injury. Elevations in bone resorption markers began at one week post injury, peaked at 16–20 weeks, and then gradually declined. At their highest value, some markers measured ten times the upper limit of normal. Given that bone loss begins shortly after injury, with the bulk of loss in BMD occurring within 4–6 months, aggressive steps should be undertaken to prevent bone loss shortly after injury [10–12].

Radiographic evidence suggests that an estimated 25 % of BMD below the level of injury is lost within the first four months following acute SCI, progressing to a 33 % loss by 16 months post injury [1, 13] and leaving patients at or near the fracture threshold [1]. Additional investigations extending the time from injury to two years estimate a BMD reduction of 30–40 % at the femoral neck, 37–52 % at the distal femur [14, 15], and 50–70 % at the proximal tibia [8, 15], with the majority of this loss occurring during the first 12 months. Bone loss subsequent to SCI occurs specifically below the level of injury. In some regions, it progresses at 1 % per week in the acute phases post injury [16]. Relative to other conditions including space travel, where losses are 0.25 % per week [17], and bed rest in otherwise neuro-intact patients, where bone loss is 0.1 % per week [18], bone loss due to acute SCI is 10–40 times greater and to date, appears to be more resistant to treatment. Intervention is needed early after injury to halt the rapid progression of bone loss, but such measures are difficult to implement given the complex metabolic factors leading to accelerated bone loss as well as medical comorbidities that may exist during the acute care phase of hospitalization.

Specifically, individuals with SCI develop sublesional osteoporosis, namely, bone loss below the level of paralysis [14]. Bone abnormalities after SCI develop at an increased rate in the following areas: proximal femur, distal femur, and proximal tibia [8, 9]. In contrast, persons without SCI exhibit higher rates of osteoporotic fractures in the axial skeleton. Areas of the appendicular skeleton in the SCI population are highly susceptible to bone demineralization due to decreased weight-bearing affecting these areas when patients are in lying and sitting positions [14].

The regional BMD in the area below the injury, rather than the overall BMD, is among the strongest predictors of future “fragility fractures” or ones that occur under conditions of minimal or low impact in the absence of trauma [19, 20]. The most significant risk factor for osteoporosis after SCI is the completeness of injury by American Spinal Cord Injury Association (ASIA) grades A through E [21], with patients who have complete injuries at greater risk than those with motor preservation below the injury level. Those with ASIA impairment A (complete) injuries as shown in Fig. 2 are more likely to experience sublesional bone loss than those with motor incomplete injuries (ASIA impairment C or D) who have retained some ability to move their lower extremities. However, having an incomplete SCI (Fig. 3) does not imply the ability to walk or even bear weight on the lower extremities. Originally developed by ASIA, this grading scheme has been adopted as the International Standards for Neurological Classification of Spinal Cord Injury. A higher incidence of sublesional osteoporosis is also observed with increasing number of years post injury [6, 22], increasing age [21, 23], female gender [24] and onset of SCI prior to age 16, when peak bone mass has not yet been achieved [14].

SCI patients with more severe injuries (complete or near-complete) are at heightened risk of developing osteoporosis, particularly if an individual is older and has a cervical level of injury, minimal spasticity, and a longer chronicity of injury [8]. The percentage of patients affected with osteoporosis is also dependent on the years since injury, gender, and neurological level of injury (cervical, thoracic or lumbar, complete or incomplete). Although bone loss inevitably occurs in the vast majority of individuals with motor complete as well as substantial numbers of motor incomplete patients with SCI, additional factors contribute to the rate and extent of bone loss below the level of injury. Apart from the severity of SCI and neurological level of injury, nutrition, lifestyle/activity levels, smoking, and family history must also be taken into account. However, these factors may be more relevant in contributing to pre-injury BMD than in preventing bone loss after SCI. The greater the deficiency in an individual’s bone density at the time of injury, the more bone a patient could theoretically lose before becoming osteoporotic.

Gifre and colleagues have developed a prediction model for development of osteoporosis 12 months after injury [25]. Their examination of 35 patients with a diagnosis of motor complete SCI of six months or less revealed that total femur BMD <1 g/cm² (RR 3.61) and lumbar BMD <1.2 g/cm² (RR 2.83) were the strongest predictive factors for development of osteoporosis by one year post injury. Both factors together suggested a probability of 96.8 % that a given individual would develop osteoporosis. Although the authors based this model on a relatively small sample, it included primarily young males with a mean age of 30, likely healthier than some populations of patients, with many still young enough not to have reached peak BMD. Overall, 52 % of their sample developed osteoporosis by one year. Other studies suggest a wide range of percentages by the first year. By patient self-report covering over 1,000 Canadians (approximately 55 % with complete injuries), 21 % stated that they had received a diagnosis of osteoporosis [26]. Given the self-report study design, this estimate is likely to be low; the results were further influenced by the inability to define the timeline of development of osteoporosis from the onset of SCI. In other investigations, prevalence of osteoporosis in SCI patients was found to be much higher; many subjects who do not reach threshold by DXA for −2.5 standard deviations below young normal by a T-score are categorized as osteopenic (T-score of −1.5 to −2.49).

In a survey by Hammond et al. involving 115 female and 264 male chronic SCI patients seen in an outpatient clinic, 34.9 % met the clinical definition of osteoporosis, while another 46.7 % were classified as osteopenic [27]. Lazo and colleagues reported a high incidence of osteoporosis in a sample of male veterans at an average of 15 years post SCI (median age of 55). In their trial, 61 % met the definition of osteoporosis, while another 19.5 % were osteopenic [28]. Perhaps the highest percentage of osteoporosis was evident in a study by Shojaei et al. of SCI veterans in Iran. In this investigation, 81.5 % demonstrated osteoporosis in the femoral neck, and another 13.1 % were found to have osteopenia. As in similar studies, the lumbar spine had lower degrees of osteoporosis due to loading in the lower back during transfers. In the lumbar lateral spine, a view which is more sensitive than the anterior–posterior view (as described in earlier chapters of this book), 16.7 % were osteoporotic while 18.2 % were osteopenic [29]. Table 1 summarizes the many investigations that have shown sublesional osteoporosis in SCI, with a mix of prospective and cross-sectional studies [15, 22, 24, 30–36].

In addition to the nutritional prevention strategies outlined earlier in this book, spinal cord injury patients have some specific risk factors for malnutrition. Low levels of serum 25-hydroxy vitamin D occur in substantial numbers of persons with acute and chronic SCI [37–41]. In humans, sunlight is the primary source of vitamin D and typically provides up to 90 % of the daily requirement [42, 43]. The capacity of a spinal cord-injured person to absorb vitamin D from the sun is limited by seasonal and related extremes of heat, cold, humidity, or dryness; skin pigmentation; functional mobility; and availability of assistance from caregivers. Individuals with tetraplegia frequently depend on others to get them out of bed, but such assistance may not be available at desired times of peak sunlight. In addition, those with injures above T6 face thermoregulatory challenges and are highly sensitive to extreme heat and humidity, while others with respiratory issues are adversely affected by very dry climates.

All persons with insensate skin are at risk of developing sunburn and those with complete spinal cord injuries are at particular risk. Although use of sunscreen with SPF >8 will block harmful ultraviolet rays and prevent such burns, cutaneous production of vitamin D3 is reduced by more than 95 % [42–44]. In most climates of the United States, exposure to sunlight for only 15 minutes between 10 am and 3 pm in spring, summer, and early fall is sufficient to obtain adequate vitamin D in persons with fair skin. Persons living in far northern states would incur this benefit only later in the spring or in early fall [45]. Although such limited time will not result in sunburn, some with cervical or upper thoracic neurologic levels of SCI cannot tolerate even this short period, due to temperature dysregulation related to alterations in the autonomic nervous system.

Research examining levels of vitamin D in SCI patients according to season and ethnicity has demonstrated that only 35 % of acute SCI patients injured in summer months and 16 % in winter months actually have therapeutic levels of vitamin D (>32 ng/ml). The remainder required supplementation to achieve therapeutic levels. Findings are summarized in Table 2 [39].

In patients with SCI, the primary goal is fracture prevention. Among those with chronic SCI, 25–49 % ultimately experience a fragility fracture [49, 50]. For patients who are unlikely to ambulate, conservative treatment with a soft splint has given way to more aggressive intervention. Untreated fractures in all sites below the level of spinal cord injury can be complicated by increased spasticity, autonomic dysreflexia, and limb deformity after healing that make transfers more difficult not just during the fracture recovery period but long afterward [51]. Femoral neck fractures heal poorly and are among the most challenging to treat. Healing is complicated by bone instability and migration of the pelvis proximally, causing pelvic obliquity, altered sitting balance, and ultimately ischial pressure ulcer development. Plaster casts have been shown to cause skin breakdown unknown to the patient or vascular compromise [50]. Since pinning often results in nonunion, endoprosthetic replacement is recommended but can be compromised by subluxation for adductor spasticity. If prosthetic replacement seems most beneficial for the patient, the physiatrist may wish to consider inpatient rehabilitation admission after the procedure, specifically to provide spasticity management along with prevention of autonomic dysreflexia. Pressure mapping to prevent pressure ulcers and review of safety with functional mobility, particularly transfers, would be additional goals of a rehabilitation stay.

The proximal tibia and distal femur are the locations with the greatest degree of bone loss from immobilization following spinal cord injury. In a series of nine patients with spinal cord disorders of mixed etiologies, each with at least one lower extremity long bone fracture, Sugi et al. [52] demonstrated superior patient outcomes relative to earlier studies. All nine subjects returned to their prior functional baseline at their final post-op outpatient visit. No participants experienced a perioperative or postoperative complication, including nonunion or infection. Significant improvement in life satisfaction was observed postoperatively, using the spinal cord injury quality of life measure. With the combined effects of an increased life expectancy after SCI and greater fracture incidence in persons over age 55, the cost physically and emotionally to the patient and financially to the patient and healthcare system will rise in the coming years [10–12, 53, 54]. Given the increasing availability of robotic ambulation devices and assisted-walking technologies involving full-body bracing, patients with complete paraplegia may be candidates for a walking program. Participation will be possible only for those subjects with reasonable bone density who have no contraindications of active unstable fractures.