A case-control study was performed by Citak et al. (2012) among 132 individuals with traumatic spinal cord injury and 132 controls to determine risk factors for HO. The authors reported that the presence of complete neurological deficit was a major risk factor for HO. Moreover, factors such as spasticity, pneumonia, thoracic trauma, tracheostomy, nicotine use, and urinary tract infection increase patients’ risk for HO (Citak et al. 2012). Contrary to previous belief, the authors reported that patients with less comorbidities were also at a higher risk for developing HO. The evaluation of the preceding factors, in combination with early intervention and diagnosis, may reduce incidence of HO or improve a patient’s recovery post-operatively (Citak et al. 2012).
Krauss et al. (2014) reported that males were five times more likely to develop HO and SCI severity is also a risk factor with AIS A patients at greater risk than AIS D patients. Injury severity was also highlighted by Ranganathan et al. (2015) whose literature review revealed that severity and level of injury with injuries to the thoracic and cervical spine are greater risk of developing HO. However, both gender and injury severity as risk factors have been disputed in the literature (Krauss et al. 2014).
Krauss et al. (2014) also investigated the role of hyper-coagulable states and related blood markers as risk factors in the development of HO. D-Dimer was elevated in 24 out of 32 patients with SCI and concurrent HO. Following this, the role of deep vein thrombosis (DVT) and pulmonary embolism (PE) have also been linked to the development of HO. Reznik et al. (2014) also reported that DVT/PE were significant predictors of HO along with multiple pressure ulcers and AIS B severity score. Reznik et al. (2014) propose that the association of HO and DVT/PE is due to the link between trauma, surgery and fractures and thrombogenic factors such as thromboplastin or factor III in the body becoming stimulated and increased. Regarding the association of HO and pressure ulcers, it is postulated to be due to pressure ulcer infection deep enough to reach the bone along with tissue hypoxia, prolonged immobilization and muscle trauma (Emami Razavi et al. 2015). Further research is required to establish the relationship between HO and pressures sores/ulcers.
After three-12 weeks, symptoms of HO start to appear (Schuetz et al. (2005). The initial clinical signs of inflammation are non-specific for HO (Neal 2003). Individuals typically present with joint and muscle pain, parasthesias and tissue swelling in the involved region, accompanied by a mild fever (Thomas & Amstutz 1987; Orzel & Rudd 1985; Smith 1998; Shehab et al. 2002). Conversely, some SCI patients do not experience any pain. Skeletal bio-markers can help detect development of HO, in particular, ALP serum, CPK, C-reactive protein, prostaglandin E2, and erythrocyte sedimentation rate which have been to be associated with HO after SCI (Ploumis et al. 2015).