Peripheral Nerve Injury and Repair Principles



Peripheral Nerve Injury and Repair Principles


D. Nicole Deal

Patricia A. Drace



INTRODUCTION



  • Pathoanatomy



    • Epineurium1,2,3



      • Circumferentially organized connective tissue layer in between and around fascicles for nourishment and protection


    • Perineurium



      • Circumferentially organized around each fascicle


      • Forms blood-brain barrier and contributes to tensile strength


    • Endoneurium



      • Loose collagen matrix, longitudinally organized within fascicles


      • Protection and nourishment of axons


    • Fascicles



      • Divide and unite to form plexuses3


      • Fascicular matching important for repair


    • Blood supply



      • Anastomosis of blood vessels2



        • Two major arterial systems



          • ▲ Superficial


          • ▲ Interfascicular epineurium—microvessels



            • image Trauma increases permeability


            • image More susceptible to compression trauma than endoneurial vessels, which can lead to intrafasicular edema and secondary nerve injury


        • One longitudinal system



          • ▲ Within endoneurium and perineurium3


          • ▲ Endoneurial capillaries function as blood-brain barrier



            • image Disrupted by toxin, ischemia, trauma, histamine, serotonin



  • Mechanism of injury



    • Stretch—most common



      • Commonly associated with motor vehicle collision (MVC)


    • Compression/ischemia


    • Transection/laceration—30%1



      • Glass, knife, fan, saw, auto metal, long bone fracture


    • Blast—complex injury with soft tissue and often vascular involvement, may involve shrapnel



      • Often necessitates fasciotomy following arterial repair


  • Epidemiology



    • Consecutive study of all peripheral nerve injuries in 2006 found 73.5% occurred in upper extremity4



      • Ulnar nerve most commonly injured


      • Combined lesions usually involve ulnar and median nerves


      • Most common cause of injury—MVC


    • Crush injury most likely type of limb injury to be associated with peripheral nerve trauma (1.9% of extremity trauma)5


    • Limb dislocation confers 1.46% rate of nerve injury5


    • Some studies show equal rates of peripheral nerve injury in males and females, whereas others show male predominance of up to 83%5,6


    • 83% of peripheral nerve injuries at the time of limb trauma are patients younger than 55 years5


    • Upper extremity injury—radial nerve injury most common followed by ulnar and median nerves6


    • Traumatic brain injury present in 60% of peripheral nerve injury patients6


  • Nerve injury physiology1



    • Transection of axons results in



      • Cell body edema


      • Shift in metabolism from synthesis of neurotransmitter to production of structural materials


      • Traumatic degeneration—proximal axon stump degenerates to node of Ranvier or even to cell body


      • Wallerian degeneration—distal axon stump and myelin degenerate in a retrograde manner



        • 48 to 96 hours after injury


        • Schwann cells mediate phagocytosis of myelin and axon debris


      • Loss of blood-brain barrier



        • Injured nerve exposed to proteins, which act as antigens and may lead to autoimmune reaction



  • Nerve regeneration physiology



    • Schwann cells support axon regeneration1



      • Begin to divide within days of injury


      • Cell linings contain nerve growth factor receptors


      • Cytokine-mediated process (interleukin [IL]-1, IL-6, transforming growth factor beta) along with macrophages as part of inflammatory process


    • Axon growth cone makes way for neurite growth



      • Axons that cannot find distal stump grow into surrounding tissues or become disorganized scar/neuroma


      • Axons that reach distal stump have reasonable chance of reaching distal target organ


      • Axon growth average 1 mm/d


    • Distal reinnervation



      • Occurs by three mechanisms1



        • Remyelination


        • Collateral sprouting distally from preserved axons


        • Regeneration from site of injury


      • Functional reinnervation needs to reach target organ by 12 to 18 months in order to allow for recovery prior to fibrosis


      • Sensory and motor end organs degenerate over time (1+ years)



        • Earlier reinnervation yields improved functionality


EVALUATION



  • History



    • Straightforward wound—laceration, no significant contamination



      • Primary repair is preferred


    • Wound with extensive tissue damage—gunshot wound (GSW), penetrating trauma with extensive soft tissue and/or vascular injury, contaminated wounds



      • Extent of nerve damage cannot immediately be assessed until the wound declares itself.


    • Closed traction injury—can have variable presentation



      • Worse outcomes with situations associated with scapulothoracic dissociation where nerves and vessels can be significantly disrupted and retracted



  • Physical examination



    • Sensory examination—altered sensation in the distribution of affected nerve



      • Test sensation to light touch, pain/pinprick, and temperature as best as possible


      • Tinel sign1—useful in following patients over time with nerve injury



        • Over area of lesion in first-degree injury


        • Generally moves distal at 1 in/mo during recovery of second-degree lesions


        • Third-degree lesions—weaker Tinel sign that recovers slower than expected


        • Fourth- and fifth-degree lesions—Tinel sign never moves distally


    • Motor examination—weakness, paralysis of muscles innervated by affected nerve



      • Test all muscles distal to the injury site innerved by affected nerve for motor strength


    • Skin changes—skin loses vasomotor tone, anhidrosis


    • May have ischemia in the vicinity of injury/affected nerve if vascular supply is damaged at the time of injury


  • Imaging—In the case of nerve injury, electrodiagnostic testing is the most useful adjunctive test available and is basically an extension of the physical examination.



    • Electromyography/nerve conduction velocity (EMG/NCV)—often more sensitive for return of function than physical examination and can contribute significantly to understanding of nerve injury and severity. See Table 36.1 for EMG/NCV findings.



      • EMG—tests muscle response to stimuli by insertion of needle into muscle to record electrical response of neighboring motor units.




        • First evidence of recovery is return of motor unit action potentials on needle examination of muscle innervated closest to site of injury.1


        • Acutely, EMG cannot determine degree of injury except complete versus incomplete lesions.



          • ▲ EMG performed at 2 weeks or earlier is useful only for exact localization of injury, not for determination of injury severity.


        • Can see recovery response on EMG weeks to months before clinical contraction is visible.


      • NCV—tests peripheral nerve response to stimuli



        • Confirms clinical examination and useful in localization of lesion


        • Results highly sensitive but can be nonspecific


        • Preserved for 7 days after nerve injury so avoid testing immediately after injury


        • Neuropraxia (see Table 36.1):



          • ▲ Compound muscle action potential (CMAP) and nerve action potential (NAP) distal to lesion are maintained indefinitely so distal stump continues to conduct


          • ▲ Proximal to the injury, may have partial or complete conduction block


        • Axonotmesis and neurotmesis (see Table 36.1):



          • ▲ EMG findings depend on timing from injury:



            • image Immediately after injury, no changes at neuromuscular junction but conduction block may be present with proximal stimulation


            • image 9 to 11 days postinjury will illustrate loss of CMAP and NAP, distal stump no longer conducts.


            • image Wallerian degeneration complete at 1 to 2 weeks



              • Degree of axon loss versus demyelination can be determined at this point.


        • EMG/NCV timing:



          • ▲ Study at 7 days can localize lesion and can tell only complete versus incomplete injury


          • ▲ Study at 2 weeks can differentiate neuropraxia versus axonotmesis and neurotmesis


          • ▲ Study at 3 to 4 weeks after fibrillation potentials have developed provides greatest amount of information1


          • ▲ Study at 3 to 4 months may detect early reinnervation


    • Radiographs—can be useful in certain cases



      • Bony stability required for appropriate nerve treatment



      • Scapulothoracic dissociation concerning for brachial plexus injury


    • Magnetic resonance imaging (MRI)



      • Can identify nerve discontinuity at the fascicular level, verifying the need for surgical repair7


      • MRI can be used for early detection of acute axonal nerve lesions



        • Nerve hyperintensity on T2 MRI is present at 24 hours following denervation, which precedes EMG spontaneous activity by 24 hours.8


      • Can be useful to determine muscle denervation after nerve injury


    • Ultrasound—Can be used to determine nerve continuity and to some degree extent of injury (accuracy of nerve injury classification 93.2%)9


  • Nerve injury classification (see Table 36.2)

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May 7, 2019 | Posted by in ORTHOPEDIC | Comments Off on Peripheral Nerve Injury and Repair Principles

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