• Every year, traumatic brain injury (TBI) contributes to a substantial number of deaths and permanent disability.  Often, a traumatic brain injury does not occur in isolation to other traumatic injuries to other parts of the body.  For example, a TBI is often a part of an acute poly-trauma, in which a person suffers multiple serious injuries at once, such as a head injury and fracture to one or more bones in the leg (femur, tibia, fibula) from a car crash.[1]

    A September, 2016 study shows a correlation between poly-trauma patients suffering from TBI and bone fractures to a different part of the body actually results in quicker speed of healing for the bone fractures.[2]   This has long been a theory,[3] but now researchers believe they have isolated the cause:  Hypoxia-Inducible factor 1-a (HIF-1a)

    How the study was done:

    The study was done at a University Hospital over the course of three years and involved 58 patients.  Of those patients, 25 had long bone fractures (femur, tibia or fibula) and were also diagnosed with TBI.  All fractures were treated with surgery.  Serum samples were taken over a period of six months and x-rays were taken at regular intervals.  The researchers found that the group with a diagnosis of long bone fracture and TBI had a shorter time to union of the bone than the other group that did not have TBI.

    Here is how the researchers believe why it works:

    During a bone fracture, the local blood vessels that innervate the bone are also immediately severed, causing a hematoma which isolates the area from perfusion.  The healing process begins by increasing a specific set of genes[4] which are responsible for anaerobic energy metabolism and matrix synthesis of the fracture repair process.  These target genes are under strict control of a newly identified transcription factor, hypoxia-inducible factor-1 (HIF-1), which has two sub-parts, a and b.  The researchers believe that the elevated HIF-1a serum levels in the TBI group with fracture was due to the flow of newly formed HIF-1a from the injured brain into the circulatory system from injured neural tissue or as part of a central nervous system response to brain injury.

    The researchers did stress that this study alone is not sufficient to draw too many conclusions and that more research is needed with a larger study group to identify the exact mechanism for how the nervous system controls bone remodeling.

    The consequences of this study may have an impact on injured poly-trauma patients who also have a personal injury claim, as the presence of TBI may explain an unexpected recovery time from fractures.  While the study confirms a faster bone fracture healing rate for those that also have to endure a traumatic brain injury, it does not in any way suggest that those poly-trauma patients recover faster from the brain injury related symptoms, or other non-fracture poly-trauma injuries, than TBI patients without fractures.

    The attorneys at Adler Giersch stay current on medical research that impacts our understanding of trauma and personal injury cases as it allows us to better advocate for our clients. Effective and tough advocacy happens best when we connect the medical-legal worlds on behalf of those with traumatic injuries caused by the negligence or recklessness of others.  If we can assist with a complimentary consultation simply give us a call.


    [1] National Hospital Discharge Survey (NHDS), 2010; National Hospital Ambulatory Medical Care Survey (NHAMCS), 2010; National Vital Statistics System (NVSS), 2010. All data sources are maintained by the CDC National Center for Health Statistics.

    [2] Sang, et al.  Elevated levels of hypoxia-inducible factor-1α in patients with fracture and concomitant traumatic brain injury.  Annals of Clinical Biochemistry 2016; ACB-16-211.R1.

    [3] Bidner SM, Rubins IM, Desjardins JV, et al. Evidence for a humoral mechanism for enhanced osteogenesis after head injury. J Bone Joint Surg Am 1990;72(8):1144-9.

    [4] heme oxygenase-1 (HO-1), vascular endothelial growth factor (VEGF), inducible nitric oxide synthetase (iNOS) and leptin.


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