The vast majority of current evidence supports the importance of addressing fracture risk after SCI since there is a higher incidence of fragility fractures in this population (Table 1). The majority of fragility fractures occur following transfers or activities that involve minimal or no trauma (Comarr et al. 1962; Ragnarsson & Sell; 1981; Freehafer 1995; Akhigbe et. al 2015) where the distal femur and proximal tibia (knee region) are most at risk.
Recent findings from review studies in veterans (n=12,162) with SCI have found that 82.6% of all fractures were at the tibia/fibula, femur or hip (Fig 1). Further, individuals with SCI were less likely to receive surgical intervention, than people without SCI, although those with SCI who have surgery did not have increased mortality or adverse event rates (Bishop et. al, 2013; Bethel et. al, 2015). Delayed fracture union is common after SCI (Grassner et al. 2017). Following a fracture there is a five-year increased risk of mortality (Pelletier et al. 2014; Carbone et al. 2014).
Figure 1. Many of the fractures that individuals with SCI sustain occur in the region of the metaphysis and epiphysis. Source: http://sci.washington.edu/info/forums/reports/osteoporosis.asp#dx
Risk factors for fragility fracture after SCI include:
- Age at injury
- Time Post-Injury
- Type of impairment
- Low BMI
- Low knee region BMD, and
- Use of anticonvulsants, heparin, or opioid analgesics.
Women are at greater risk compared to men (Vestergaard et al. 1998; Lazo et al. 2001; Nelson et al. 2003; Garland et al. 2004). Increasing age and longer TPI (Frisbie 1997; McKinley et al. 1999; Garland et al. 2004; Garland et al. 2005) increases fracture risk which rises significantly at 10 years post-injury. Further, people with paraplegia have more fractures (Frisbie 1997) and those with complete injuries have greater bone mass loss compared with those with incomplete injuries (Garland et al. 2004; Garland et al. 2005).
A number of concurrent medications a patient is taking can also decrease or substantially increase fracture risk. These include but are not limited to: heparin, benzodiazepines, anticonvulsants, proton pump inhibitors, selective serotonin reuptake inhibitors and opioid analgesics. In a large retrospective cohort study of men with chronic SCI (n=6969, ≥ 2 years post-injury), the use of thiazide-type diuretics was associated with a 25% reduction in the risk of lower extremity fragility fractures (Carbone et al. 2013c). In contrast, the use of heparin (HR 1.48, CI 1.20-1.83), opioid analgesics (HR 1.80, CI 1.57-2.06), or anticonvulsants (HR 1.35, CI 1.18-1.54), especially the benzodiazepine sub-class (HR 1.45, CI 1.27-1.65), was associated with an increased risk of lower extremity fragility fractures in men with chronic SCI (≥ 2 years post-injury) (Carbone et al. 2013a, 2013b). Men with chronic SCI are at a slightly increased risk of lower extremity fragility fractures when exposed to proton pump inhibitors (HR 1.08, CI 0.93-1.25), selective serotonin reuptake inhibitors (HR 1.05, CI 0.90-1.23), or thiazolidinediones (HR 1.04, CI 0.68-1.61) (Carbone et al. 2013a, 2013b). However, these drugs and a prior history of fragility fracture or a history of fracture in a parent are known risk factors for the development of osteoporosis in the general population, and should, therefore, be considered when assessing fracture risk in SCI patients.