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Fibrin Glue Augmentation Of Nerve Repair Does Not Impede Neurological Recovery In An Animal Model
Greg Rafijah, MD; Christina Dolores, MD; Andy Bowen, MD; Ryan Vitali, MD; Tahseen Mozaffar, MD; Ranjan Gupta, MD
Orthopaedic Surgery, University of California, Irvine, Irvine, CA

Background: Segmental nerve defect repair remains a challenge for surgeons. When this complex reconstructive surgery is performed, traditional repair techniques demand neurorrhaphy with microsuture. Fibrin glue can be employed in order to expedite the surgical procedure and help to maintain proper spatial orientation to assist optimal recovery. However, many micro-surgeons are hesitant to employ fibrin secondary to concerns of inhibiting nerve regeneration. The aim of this study was to evaluate if fibrinís inhibitory effects if any on nerve regeneration.

Methods: A critical size defect of 10mm was created in 24 Sprague-Dawley rat sciatic nerves with three different forms of repair used: group I, collagen type-I conduit (n=8); group II, collagen type-I conduit filled with fibrin glue (n=8); group III, autologous nerve graft (n=8). The conduit filled with fibrin glue group was designed to create a barrier to successful nerve regeneration.  Outcomes measured include weekly sciatic functional indices (SFI), to evaluate functional motor recovery. Terminal electromyography (EMG), immunohistochemistry (IHC), and histomorphometry including number of myelinated axons and G-ratios were used to analyze nerve regeneration at 12 weeks post repair.

Results:  The degree of regeneration and remyelination was greatest in the autograft group.  Both conduit groups demonstrated decreased axon counts with less myelination compared to controls and autograft.  Although there were some differences between the conduit groups in the number of myelinated axons and G-ratios, these differences were not statistically significant.  All repair groups experienced loss of large diameter myelinated fibers compared to control.  Over twelve weeks, all groups' motor function measured via SFI improved.  The degree of SFI recovery between conduit groups was comparable statistically, but clearly inferior to autograft.  Similarly, EMG results of conduit groups were indistinguishable amongst each other and significantly less than autograft and control.  IHC revealed macrophage levels and scarring severity in the conduit groups to be nearly identical.

Conclusions: As expected, the autograft group showed a significantly greater degree of recovery compared to the groups repaired with nerve conduit. Quite remarkably, the data show fibrin glue does not impede regeneration even when interposed as a barrier for nerve regeneration across a conduit.  In fact, there were no meaningful functional, electrophysiological, or morphometric differences observed between the two conduit groups.  As such, the data supports a surgeonís choice of using fibrin glue without having a deleterious effect on nerve regeneration.


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