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Common peroneal nerve decompression and application of NeuroCap device (Polyganics)

    Overview

    Learn the Common peroneal nerve decompression and application of NeuroCap device (Polyganics) surgical technique with step by step instructions on OrthOracle. Our e-learning platform contains high resolution images and a certified CME of the Common peroneal nerve decompression and application of NeuroCap device (Polyganics) surgical procedure.
    The superficial peroneal nerve is at risk during fasciotomy of the anterior and peroneal compartments of the lower leg. This patient sustained a complex lower limb blast injury and underwent fasciotomy surgery for compartment syndrome. The blast injury had resulted in direct trauma to the muscles within the anterior and peroneal compartments and an axonal injury (axonotmesis) to the common peroneal nerve (both the deep and superficial components). The sensory recovery in the deep peroneal cutaneous territory was good with patient reported sensation in the dorsum of the first web space at 6/10. There was anaesthesia (0/10) in the superficial peroneal territory on the dorsum of the foot, trophic changes with dry skin, small skin ulcers from repetitive trauma and severe neuropathic pain. The patient had a below knee amputation to the contralateral limb as a consequence of severe trauma from the blast injury. The pain in the residual affected limb was so severe that the patient was unable to stand. Any active contraction of the peronei, the tibialis anterior or the extensor digitorum longus would also provoke the pain. The patient had requested amputation of the affected right lower leg as a pain management intervention because he had become confined to a wheelchair for several years being unable to stand on the right leg to walk using the left below knee prosthesis.
    Diagnostic block of the peroneal nerve erradicated the pain for a few hours. A decision was made to explore for a superficial peroneal nerve neuroma and to undertake a neurolysis of the deep peroneal nerve from the distal peroneal tunnel through the scarred area past the site of Tinels’ sign.
    There is no satisfactory solution for painful neuromata. In a neuroma in continuity for a critical nerve sensory restoration through excision of the neuroma and nerve grafting may reduce neuroma pain. Restoration of pain to anaesthetic skin may modulate pain pathways centrally. Using a processed nerve allograft may confer advantages over autologous nerve grafting as the latter creates another sensory nerve injury (albeit a controlled surgical insult) to a nerve in a pre-sensitised individual. In many situations there is an end neuroma or the bed is too poor for grafting. Many operations have been described for end neuromata including repositioning the proximal end to deeper tissues with less scar including bone and muscle.
    Polyganics have developed a bio-resorbable nerve capping device (the NeuroCap) that is designed to cover the nerve end following neuroma resection. The device has a chamber for nerve regrowth but the nerve is prevented from adherence to scar by a physical barrier which slowly changes to a hydrogel and is ultimately completely resorbed over 18 months. The NeuroCap is made from a copolyester poly-lactide-caprolactone (PLCL).

    Indications

    INDICATIONS:
    The indications for exploration of a neuroma are neuropathic pain with neurostenalgia (tether pain) following trauma to a peripheral nerve that is not responsive to conservative management with analgesia, neuromodulator medication, desensitisation exercises and other strategies including mirror therapy. There should be a good response to targeted peripheral nerve local anaesthetic blockade with a pain reduction of at least 50% on a visual analogue scale. The decision to use a NeuroCap should be for the management of an end neuroma following nerve transection or amputation. The NeuroCap can also be used for the management of a neuroma in continuity in sensory nerves where there is no distal sensory preservation and there is a contraindication to reconstruction such as a poor surgical bed that is unlikely to provide a favourable environment to support regeneration through a nerve graft.

    SYMPTOMS & ASSESSMENT:
    The patient reported sever neuropathic pain in the right lower leg exacerbated by standing. Sensation was reduced in the deep peroneal cutaneous over the first webspace at 6/10. Sensation was absent in the superficial peroneal nerve territory (0/10) with trophic changes in the skin due to denervation. The skin was dry due to loss of sudomotor function and there were cracks and small areas of trophic ulceration from trauma. The neuropathic pain was mapped to the superficial peroneal nerve cutaneous territory. The area of skin in the distal 1/3 of the lower leg to the ankle demonstrated hyperaesthesia (increased sensitivity), allodynia (pain on light touch), hyperpathia (increasing pain response with repeated light touch) and hyperalgesia (heightened response to pain). The superficial peroneal nerve demonstrated a strong Tinel’s sign at the distal end of the lateral fasciotomy wound. There was a less marked Tinel’s sign over the proximal deep peroneal nerve at the proximal edge of the zone of trauma. There was no active movement in any of the anterior or peroneal compartment muscles despite reasonable bulk. Passive movement of the toes and ankle provoked pain exacerbations due to nerve tether (neurostenalgia).
    INVESTIGATION:
    Neurophysiology tests including nerve conduction studies and electromyography were poorly tolerated due to pain. Limited studies demonstrated no sensory conduction in the distal superficial peroneal nerve, reduced velocity and amplitude in the distal deep peroneal nerve and evidence of reinnervation changes in both deep and superficial peroneal muscles and confirmed a diagnosis of pseudoparalysis.
    Staged diagnostic nerve blocks were performed for the deep peroneal nerve and then the main peroneal nerve at the knee. The patient reported excellent pain relief following nerve blockade with maximum relief following the second block.
    The patient would not tolerate ultrasound examination due to pain.
    OPERATIVE ALTERNATIVES:
    There is no single satisfactory solution for definitive management of a painful neuroma. In a neuroma in continuity for a critical nerve, sensory restoration through excision of the neuroma and nerve grafting may reduce neuroma pain. Restoration of pain to anaesthetic skin may modulate pain pathways centrally. Using a processed nerve allograft may confer advantages over autologous nerve grafting as the latter creates another sensory nerve injury (albeit a controlled surgical insult) to a nerve in a pre-sensitised individual.
    In many situations there is an end neuroma or the surgical bed is too poor to sustain revascularisation and nerve regeneration through a nerve graft. Many operations have been described for end neuromata includingsimple transection of the nerve and removal of the neuroma. Regrowth and tether of the cut nerve end in scar is very common and therefore repositioning the proximal end to deeper tissues including bone and muscle is often recommended. The aim of this intervention is to provide more padding around the nerve end to prevent mechanical irritation and the healthier tissues should be better vascularised and prevent nerve tether to mobile cutaneous tissue. Allograft can be used to redirect regenerating nerve proximally or directly in to muscles in situations where the anatomy precludes direct deeper relocation of the nerve end following end neuroma resection. Polyganics have developed a bioresorbable polycaprolactone nerve capping device (the NeuroCap) that is designed to cover the nerve end following neuroma resection. The device has a chamber for nerve regrowth but the nerve is prevented from adherence to scar by a physical barrier which slowly changes to a hydrogel and is ultimately completely resorbed over 18 months.
    NON-OPERATIVE ALTERNATIVES:
    The management of neuroma pain is challenging. Patients frequently are prescribed increasing doses of systemic opioid medication with poor symptom relief. Neuromodulators including Pregabalin and Gabapentin may modulate the pain response through their effects on central pathways. The use of antidepressant medications can also help to modulate central pain perception and improve affect in patients with chronic neuropathic pain. Topical analgesics including local anaesthetic patches may help areas of cutaneous hyperaesthesia and local anaesthetic gels or creams may have the added benefit of facilitating local scar management to reduce nerve tether and desensitise nerve endings in the skin. Capsaicin patches are useful in areas of cutaneous hypersensitivity.
    Physical therapies including friction massage, desensitisation, neural glides, neural stretches and muscle strengthening are useful in rehabilitation after nerve injury. Sensory re-education can help restoration of functional use of a limb. The benefits of improved engagement on patients psychological well being is difficult to quantify but must not be under estimated.
    Electrotherapy with nerve stimulators can mitigate the effects of long standing denervation and trophism within muscles. Functional electrical stimulation and biofeedback improve functional use of muscles and assist neural regeneration. Nerve stimulation can modify the pain response and is the basis of transcutaneous electrical nerve stimulation (TENS) therapy.
    Spinal cord stimulation is an option for severe neuropathic pain management when other more conservative methods have failed and where there is no surgical target for the management of the neuropathic pain.
    Mirror therapy involves the use of masking of the affected limb and functional movement, tactile stimulation and massage of the contralateral normal limb with graduated introduction of tactile stimulation bilaterally to facilitate visual over riding of the pathological central nervous system pain pathways. This has demonstrated benefit in the management of phantom limb pain after amputation and in the rehabilitation after peripheral nerve injury and stroke.
    Following a unilateral limb injury some patients experience severe chronic neuropathic pain syndromes including causalgia and complex regional pain syndrome. Caution should be exerted regarding making such diagnoses because whilst a label may facilitate access to services, not all patients who have neuropathic pain after a nerve injury meet the diagnostic criteria for a diagnosis of CRPS Type 2 and labelling as such can have adverse psychological consequences for some patients. In patients with chronic neuropathic limb pain there is demonstrable difficulty in recognition of side when testing subjects with flashcards depicting left and right hand images. Cortical localisation training is a strategy that can be employed to improve function and prevent neglect of the affected limb.
    Psychological support and treatment strategies including mindfulness therapy, cognitive behavioural therapy and counselling may benefit patients living with neuropathic pain or struggling with the the debilitating effects of anxiety, sleep disturbance, hyper-vigilance and flashbacks that frequently result from traumatic events. Depression and post traumatic stress are specific psychiatric diagnoses that may require more specialised support from psychiatric services.
    CONTRAINDICATIONS:
    The NeuroCap is contraindicated in active infection, poor surgical beds or in patients with known hypersensitivity to polycaprolactone. The NeuroCap is limited to 8mm diameter nerve stumps and the stump should be measured so that an appropriate sized device can be used for each nerve. The nerve stump should have sufficient length that it can be mobilised and introduced to the cap with a 5mm distal void to allow for unsupported nerve regeneration. The device must be anchored loosely to a deep tissue plane to prevent superficial migration and the risk of wound irritation or extrusion. The soft tissue cover should adequate to pad the area as the NeuroCap may be palpable for a few months. Caution should be exerted in the surgical management of neuromata where there is only a poor response to pre-operative local anaesthetic nerve blockade. In such cases the pain may have significant central modulation that will result in a poor response to surgical intervention in the periphery.

    Setup

    The patient is examined and marked pre-operatively. The points of maximum Tinel’s sign are noted for the deep and superficial peroneal nerves.
    Under general anaesthesia with a thigh tourniquet the limb is prepped and draped.
    The limb is elevated at this stage prior to tourniquet inflation. This delay in tourniquet elevation ensures that the risk of tourniquet induced ischaemia (typically after 30 minutes) doesn’t impact on the deep peroneal nerve stimulation thresholds.
    The patient should have no neuromuscular blockade. Peripheral nerve blocks distant to the site of surgery are possible although I prefer to use a field block and an indwelling nerve catheter at the end of the procedure for surgical neurolysis and the management of neuromata.

    Operation – 1

    1 – Fibula head
    2 – Common peroneal nerve
    3 – Deep peroneal nerve Tinel’s sign at distal end of scar
    4 – Strongest Tinel’s sign over superficial peroneal nerve at end of scar
    5 – Hyperaesthesia and allodynia in superficial peroneal territory
    6 – Anaesthesia in superficial peroneal territory with trophic changes in the skin
    7 – Hypoaesthesia in the deep peroneal territory

    The lower end of the lateral fasciotomy scar is opened. There is dense scar between the dermis and the muscles of the peroneal compartment.

    Elevation of skin flaps and exposure of the deep fascia over the peroneal compartment.

    Medial dissection to the septum between anterior and peroneal compartments.

    1 – The septum between the peroneus longus and the extensor digitorum longus is visible.
    The superficial peroneal nerve should be exiting through this plane. Because of dense scarring the superficial peroneal nerve will later be exposed in normal tissue at the peroneal tunnel and distally in the subcutaneous tissues to avoid inadvertent injury. When the proximal and distal nerve exposure is completed the nerve can be traced into the scarred area.

    Further mobilisation of the posterior skin flap and release of muscle scar to dermis over the peroneal compartment.

    Further mobilisation of the anterior skin flap and release of muscle scar to dermis over the anterior compartment. This exposure is to identify the deep peroneal nerve and trace proximally to the Tinel’s point in this wound. The superficial peroneal nerve cannot be safely defined within this wound due to scar and will need proximal and distal exposure.

    Development of the intermuscular plane between extendor digitorum longus (EDL) and tibialis anterior withiin the anterior compartment. The distal deep peroneal nerve is identified in the plane between extensor hallucis longus (EHL) laterally and tibialis anterior medially. In the proximal wound the deep peroneal nerve lies in the plane between the EDL laterally and tibialis anterior medially.
    The distal deep peroneal nerve is tagged with a sloop to assist retraction during proximal dissection. The septum between EDL and tibialis anterior is released proximally.
    1 – EDL
    2 – Tibialis anterior
    3 – EHL
    4 – Deep peroneal nerve.

    Using a nerve stimulator on the distal deep peroneal nerve to detect stimulation thresholds prior to neurolysis. The stimulation thresholds are higher than normal at 3mA

    The blue sloop is tagging the deep peroneal nerve
    1 – Nerve to EHL
    2 – Deep peroneal nerve
    3 – Anterior tibial vessels

    There is scar thickening in the fascia around the deep peroneal nerve at the level of the proximal Tinel’s sign. The fascia is released and the neurolysis of the nerve completed. There is no evidence of a neuroma in continuity and given the intact motor function on electromyography and relatively normal distal deep peroneal sensation the neurolysis is sufficient for this nerve.
    1 – Main deep peroneal nerve trunk distal to tibialis anterior innervation
    2 -Maximum Tinel’s sign
    3 – Maximum point of scar over nerve which has been released.
    There is still tether on the deep surface of the nerve which will be released as the neurolysis is completed in a proximal direction using the blue sloop to gently lift the nerve.

    The deep peroneal neurolysis has been completed and the stimulation thresholds are now normal at 0.2mA. The deep peroneal nerve is tagged in the medial aspect of the wound with a yellow sloop.
    The wound is now extended distally beyond the original fasciotomy scar and the sensory component of the superficial peroneal nerve (SPN) is tagged with a white sloop.

    At the end of the scar there is abundant fibrosis circumferentially around the SPN. A neurolysis is performed using the white sloop for retraction on the nerve.

    The SPN is traced proximally into the PL/EDL interval.

    At this point there is lots of scar and the SPN appears thickened consistent with a neuroma. This point correlates well with the maximum Tinel’s sign over the SPN.

    The neuroma is seen within the SPN in scar.

    Neurolysis around the neuroma at the point of maximum Tinel’s sign over the SPN.

    The neuroma in continuity within the SPN is fully mobilised. The nerve diameter is being measured to choose the optimum NeuroCap size. In this case 3.5mm diameter. The neuroma has no distal preserved function and the decision to resect and cap was made because of the extensive scar and the probability of poor functional recover through a graft and the risk of further sensitisation.

    The blue sloop marks the neurolysed DPN and the white sloop the neuroma in continuity in the DPN. Bothe the sites of pathology correspond with the sites of maximum Tinel’s sign on careful pre-operative clinical assessment. Accurate marking pre-operatively is essential to guide the surgeon to the pathology.

    The SPN neuroma on a microsurgery background prior to resection.

    The neuroma is sectioned from the distal nerve stump. There was no sensation pre-operatively so although there was some anatomical continuity it is to all intents and purposes an end neuroma. The reconstructive option include excision of neuroma and interposition graft or resection of the neuroma and burying of the proximal stump.
    Caution should be exercised in reconstructing a neuroma in continuity. Use of another sensory nerve to bridge the gap creates another site of nerve injury in a neuropathic pain sensitised individual. Processed nerve allograft is a useful alternative in such situations however the surgical bed is poor and the longstanding nature of the injury makes it unlikely that useful function will be achieved and reconstruction would also carry the risk of creating hyperaesthesia and allodynia on the dorsum of the foot where it is currently numb with minimal functional consequences for the patient.

    The neuroma has been resected and sent for histopathological analysis.
    The cut end of the proximal nerve is introduced to a 3.5mm NeuroCap using an 8’0 nylon mattress suture. The cap is trimmed to fit but a chamber of at least 5mm should be left as a void between the nerve stump and the end of the NeuroCap to allow for axon sprouting.

    Th eNeuroCap is tagged loosely into position to a deep fascial plane to prevent superficial displacement. The cap is placed distal to the motor branch to EHL.

    The peroneal tunnel was irritated pre-operatively with some evidence of slowing on neurophysiology. This was also a site of pain for the patient. Due to the distal pathology a decompression was discussed to avoid any “double crush” concerns.

    The common peroneal nerve (CPN) is exposed within the peroneal tunnel at the fibula neck. The nerve is closely apporximated to the bone and care should be taken when exposing here as the nerve is very superficial. The nerve can be identified proximally posterior to the biceps femoris insertion on the fibula head for surgeons not familiar with this anatomy. The more proximal exposure is safer for the inexperienced surgeon, although the patient is best positioned in the lateral position to gain access more posteriorly.
    Using this exposure the proximal decompression can be performed for 3cm using a Langenbeck retractor in the proximal wound edge to expose the mouth of the peroneal tunnel and release to the level of the biceps femoris insertion.

    Operation – 2

    A Mixter is passed deep to the CPN

    A sloop is retrieved in the Mixter taking care not to trap epineurium and the sloop is delivered. This will allow gentle retraction of the nerve and minimise handling.

    The CPN is neurolysed and traced distally towards the arching fascial connections between the peroneus longus origin from the upper fibula and the proximal origin of the EDL from the lateral tibia.

    The nerve is retracted and the arch is lifted before sectioning of the fascia to decompress the nerve.
    1 – EDL origin
    2 – PL origin
    3 – CPN

    1 – The deep fascia on the undersurface of the EDL must be released to decompress the nerve. The muscle can be left intact.

    A nerve stimulator is used to map the SPN and DPN components and measure the stimulation threholds prior to releasing the distal septum over the DPN between the EDL and the tibialis anterior.

    1 – CPN
    2 – SPN
    3 – Nerve to peroneus longus
    4 – DPN
    The Jamieson’s scissors are being used to neurolyse the loose interfascicular epineurium between the proxiaml articular branch to the tibio-fibular joint and the more distally located tibialis anterior motor branch of the deep peroneal nerve. During release of the proximal peroneus longus extreme care should be taken to avoid trauma to the peroneus longus branches. Normally there are least 2 branches visible within the peroneal tunnel decompression.

    The individual branches are mobilised and tagged with sloops to insulate them from the other branches for identification with nerve stimulaton and detection of stimulation thresholds.

    Nerve stimulation on the tibialis anterior branch after release of the tight overlying septum. I excise a piece of this septum to prevent further compression.
    1 – Articular branch
    2 – Tibialis anterior branch
    3 – EDL branch overlying the reminder of the DPN

    The completed surgical exposure with CPN decompression, neurolysis of the DPN and resection of neuroma and capping for the SPN in a single incision.

    A nerve catheter is sited at the peroneal tunnel for local anaesthetic bolus on wound closure. A background infusion can be run for 48 hours with intermitted bolus as needed to maintain a block of the peroneal nerve to help in post-operative pain management. Supplementary local anaesthetic can be infiltrated to the wound edges.
    The wound is closed with subcuticular absorbable suture, steristrips and an occlusive dressing.
    A bulky wool and crepe bandage is applied to support the wound and provide a moderate compression to minimise the risk of post -operative haematoma.

    Post Operative

    The patient had significant neuropathic pain and so an inpatient stay was planned for post-operative pain management with a local anaesthetic infusion around the common peroneal nerve for 48 hours.
    Subcutaneous heparin was administered at the end of the procedure and will be continued until the patient is mobile.
    The limb should be kept elevated on pillow for 48 hours and for 1 week when at rest.
    The nerve catheter is removed after 48 hours when the patient’s analgesia requirements are stabilised.
    The dressings can be reduced at 1 week and the wound inspected. A further light occlusive dressing is maintained until wound healing at 2 weeks when the steristrips are removed.
    I recommend continuing with neuromodulatory agents as used pre-operatively until the 6 week clinic review when they can be slowly weaned over the next 3 months if pain control is adequate.
    The NeuroCap is subject to evaluation in a clinical trial and functional scores and visual analogue pain scores plus opiate and neuromodulatory requirements are monitored for 2 years post-operatively.

    Recommended Reading

    The patient should have a visual analogue score monitored pre-operatively, after the diagnostic block and at intervals of 3,6,12 and 24 months post-operatively. The outcome of neuroma surgery is variable. Careful pre-operative patient assessment and selection is key to good results.
    References:
    Van Der Avoort DJJC, Hovius SER, Selles RW, Van Neck JW, Coert JH. The incidence of symptomatic neuroma in amputation and neurorrhaphy patients. J Plast Reconstr Aesthetic Surg. 2013;66(10):1330-1334
    Stokvis A, van der Avoort D-JJC, van Neck JW, Hovius SER, Coert JH. Surgical management of neuroma pain: a prospective follow-up study. Pain. 2010;151(3):862-869
    Lewin-Kowalik J, Marcol W, Kotulska K, Mandera M, Klimczak A. Prevention and management of painful neuroma. Neurol Med Chir (Tokyo). 2006;46(2):62-67; discussion 67-68
    Watson J, Gonzalez M, Romero A, Kerns J. Neuromas of the hand and upper extremity. J Hand Surg Am. 2010;35(3):499-510
    Elliot D, Sierakowski A. The surgical management of painful nerves of the upper limb: a unit perspective. J Hand Surg Eur Vol. 2011;36(9):760-770

    Reference

    • orthoracle.com

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