Journal of orthopaedic research : official publication of the Orthopaedic Research Society
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Pedicle screws for spinal fixation risk neural damage because of the proximity between screw and nerve root. We assessed whether spinal somatosensory evoked potential (SSEP) could selectively detect pedicle-screw-related acute isolated nerve injury. Because pedicle screws are too large for a rat's spine, we inserted a K-wire close to the pedicle in 32 rats, intending not to injure the nerve root in eight (controls), and to injure the L4 or L5 root in 24. ⋯ SSEP monitoring provided reliable, useful diagnostic and intraoperative information about the functional integrity of single nerve-root injury. These findings are clinically relevant to acute nerve-root injury and pedicle-screw insertion. If a nerve-root irritant remains in place, a considerable neurologic deficit will occur.
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The etiology of local posttraumatic infection in the locomotor system depends on the amount, virulence and pathogenicity of the inoculated microorganisms and the local/systemic host damage due to the type and extent of the accident or iatrogenic trauma. The relative effect of these factors remains unclear. In particular, it is still unclear today whether--in presence of microorganisms--soft tissue damage and its pathophysiological consequences lead to infection after soft tissue trauma, or whether the bacterial contamination is the primarily cause for posttraumatic infection. The aim of the project was to gain information on the consequences of a soft tissue injury in terms of resistance to local infection. Since clinical populations are too heterogeneous, the problem was investigated in a standardized, reduced (no surgery or implants) experimental in vivo model. ⋯ The infection rate after a standardized closed soft tissue injury was significantly higher and the ID50 lower than without soft tissue trauma. Our results demonstrate that in presence of microorganisms it is not primarily the bacterial contamination but rather the soft tissue damage and its pathophysiological consequences resulting in decreased infection resistance that secondarily lead to infection.