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Suprascapular nerve decompression and reconstruction

    Overview

    Learn the Suprascapular nerve decompression and reconstruction surgical technique with step by step instructions on OrthOracle. Our e-learning platform contains high resolution images and a certified CME of the Suprascapular nerve decompression and reconstruction surgical procedure.
    A 35 year old man was referred to the regional peripheral nerve injury service 10 months after a heavy blow to the front of the left shoulder during a fall from a mountain bike during an off road descent. Plain radiographs of the clavicle and shoulder were reported as normal. He was rehabilitated with physiotherapy. After 3 months there was useful abduction using deltoid but no evidence of supraspinatus function and he was referred for an ultrasound of the rotator cuff to exclude a tear. The ultrasound was normal showing mechanical integrity of the muscle-tendon unit. Further rehabilitation was advised. The treating physiotherapist highlighted weak abduction and external rotation and a diagnosis of suprascapular nerve neurapraxia was made. No neurophysiology was requested to confirm this diagnosis. He was not improving by 9 months with weak overhead activity and poor external rotation and he was referred to the nerve unit for assessment.
    He was assessed 10 months after the injury and there was no function in the supraspinatus or infraspinatus with wasting of both muscles. There was deep seated pain over the suprascapular nerve on palpation. The remainder of the brachial plexus examination was normal. There was no Tinel’s sign at the upper trunk which would have been suggestive of an avulsion of the suprascapular nerve take-off at this level. However the suprascapular nerve is has no cutaneous sensory territory and Tinel’s sign for a rupture is therefore unreliable. A diagnosis of traction injury or distal rupture of the suprascapular nerve was made and he was listed for urgent exploration the next day. Intra-operative neurophysiology was planned to avoid further delay. Effective reinnervation in a proximal rupture will only be achieved with a nerve transfer at this stage. The time of presentation is too late for a proximal graft reconstruction to provide useful reinnervation by 12 months. The best option for the patient would be to identify evidence of traction injury with axonopathy and regeneration complete but non-functioning due to persisted segmental conduction block at a tight suprascapular ligament. In such cases stimulation improves after decompression of the ligament and further expectation of recovery and strengthening for 6-12 months would be anticipated. If a short segment rupture is identified at the suprascapular notch this would be amenable to a graft. Otherwise the recommended treatment would be a decompression, stimulation assessment and consideration given to a nerve transfer.
    At surgery there was a tight ligament but no stimulation and no neuroma at the area exposed. A working diagnosis of a more proximal rupture was made and a distal nerve transfer from the medial branch of the XIth cranial nerve was performed just proximal to the suprascapular notch.

    Indications

    INDICATIONS
    This is an unusual case where there has been a blow against the shoulder and loss of suprascapular nerve function in isolation. This implies that there is a traction injury with axonopathy or a rupture as there is no functional recovery at 10 months. The patient was referred late and so now there is an imperative to restore function in the nerve as quickly as possible. There is no sensory territory to confirm the diagnosis so EMGs for the supraspinatus and the infraspinatus are useful to confirm denervation and an ultrasound of the rotator cuff to exclude complex cuff tear to supraspinatus and infraspinatus to explain the paralysis. The imaging was done by way of exclusion in the shoulder clinic and a late referral was due to the expectation of recovery with an inaccurate early pathophysiological nerve injury diagnosis of a neurapraxia.
    The aim of surgery was to expose the nerve, decompress at the notch and stimulate. If there was retained function then further monitoring would be appropriate. With no function the options are identify the damaged segment and graft or distal nerve transfer from the medial XI branch. In this case the late presentation meant that there was insufficient time for a graft to regenerate to the muscle so if needed a nerve transfer would be be used for reconstruction.
    The main indication for a nerve transfer to the suprascapular nerve (SSN) is following a C5 avulsion injury. In this situation there is no proximal nerve stump available for grafting and so a nerve transfer provides a reliable way of restoring innervation to the denervated muscles. The transfer is performed close to the motor point of the supraspinatus and therefore reinnervation is rapid. The same technique can be used for upper trunk ruptures with late presentation where graft reconstruction of the upper trunk is unlikely to restore motor function to the supraspinatus due to the time-distance phenomenon of nerve regeneration. In cases where the upper trunk has been grafted early but failed to recover, this nerve transfer can be used as a salvage procedure.
    The timing of nerve transfer is critical and generally speaking the earlier the transfer is performed the better the results. In avulsions and other un-reconstructable lesions, no recovery can be expected and early nerve transfer is indicated. In cases where there is a potential for spontaneous recovery, a period of observation is usual. Nerve transfer can be deferred in this instance, but needs to be performed ideally at between 6 to 9 months following the injury, if successful reinnervation of the supraspinatus and infraspinatus is going to be achieved by 12 to 18 months.
    I also use this technique for other causes of C5 nerve root dysfunction. In cases of brachial neuritis (Parsonage-Turner syndrome) with no supraspinatus recovery by 9-12 months, this technique can be employed for reinnervation as long as the XIth nerve is functioning. There is a small risk of a further episode of neuritis as a response to surgery. The aetiology is poorly understood but probably represents an autoimmune response to viral insult in a sensitised individual.
    I also use this technique for restoration of function in patients with a non-reversible motor radiculopathy associated with degenerative cervical disc disease. The timing is controversial because, unlike traumatic avulsions, typically these lesions are incomplete and may have some potential for spontaneous regeneration. Such incomplete lesions may exhibit longer windows for surgery due to the fact that intact axons within the nerve may auto “babysit” the motor end plates and collaterally sprout to denervated muscle fibres. There may be too few axons for function but the paralysed muscle may be able to respond to reinnervating axons for longer than the 12 months typical of a complete peripheral nerve injury.
    SYMPTOMS & EXAMINATION
    In this case there was loss of innervation in the suprascapular nerve (SSN) territory in isolation resulting in paralysis of the supraspinatus and the infraspinatus. The rest of the brachial plexus function was normal. There was tenderness over the SSN at the level of the suprascapular notch but no Tinel’s sign in the neck or along the course of the SSN. there is no sensory territory for the SSN and the sensation was intact in this case. Shoulder abduction was weak with fatigue. External rotation in the abducted position was weak but intact with teres minor functioning. There was no external rotation in the adducted shoulder position. these clinical findings suggest isolated loss of the SSN function with a differntial diagnosis of a complete tear of the supraspiantus and infraspinatus tendons. A more common cause of loss of SSN is as part of a brachial plexus injury with either a C5 avulsion or a rupture of the upper trunk (C5 and C6 loss).
    In a C5 avulsion there is loss of shoulder abduction and external rotation with complete paralysis of the supraspinatus, infraspinatus, deltoid and teres minor. Levator scapulae and the rhomboid muscles are generally paralysed because the dorsal scapular nerve takes origin proximally on the C5 root. If these 3 medial scapula muscles are preserved it may suggest that the C5 root is ruptured, however these muscles may receive innervation from C4 in a pre-fixed brachial plexus and so integrity of these muscles does not guarantee that a proximal C5 nerve stump is available for grafting.
    In cases of C5 and C6 loss there is complete loss of the above muscle plus additional loss of the subscapularis, teres major, clavicular head of pectorals major, biceps, brachialis and brachioradialis. Serratus anterior will be weak but there is still some innervation through the C7 root.
    The shoulder will be held in adduction and internal rotation (C5) with the elbow in the extended position (C5 and C6). Functionally this is devastating for patients because in a partial plexus injury the intact forearm and hand cannot be positioned in space to allow environment interaction. Nerve transfer reconstruction is ideal for this injury because reconstruction is performed using donor expendable nerve branches or redundant motor fascicles from within intact nerves originating from the lower plexus and traversing the neck and shoulder regional in close proximity to the paralysed muscles before reaching their targets in the forearm and hand. This anatomical relationship renders them ideal for functional reinnervation of the shoulder and elbow. In contrast isolated lower brachial plexus injuries with preserved shoulder and elbow function are less suitable for nerve transfer reconstruction because the reinnervation distances are longer from the donor motor branches.
    Sensory loss of the outer upper arm to the elbow (C5) and the radial forearm and hand palmar and dorsal aspects (C6) is readily demonstrated.
    Passive range of motion of the shoulder must be assessed because longstanding loss of C5 function results in adduction and internal rotation contractures. Therapy should be directed to restoring passive range and the shoulder can be manipulated at the time of anaesthesia for the nerve transfer surgery. Early reinnervation with weak muscles are not able to maintain the range achieved through manipulation and therapy and so an extended rehabilitation is required until there is sufficient power in the recipient muscles to maintain range of motion. As the nerve transfer recipient muscle strength increases the patient can work to and gradually beyond the range achieved with physiotherapy. Further improvements in strength, range off motion and function are expected to 2 years and beyond.
    IMAGING
    A plain radiography may demonstrate fractures and dislocations around the shoulder girdle in the context of trauma. CT scan performed later may demonstrate calcification of the suprascapular ligament, which is a rare cause of this pattern of weakness. Ultrasound or MRI may demonstrate a ganglion from the superior labrum of the shoulder impinging on the suprascapular nerve.
    An ultrasound is the treatment of choice for diagnosis of a cuff tear. In this case the cuff was intact and no further investigations were requested. An MRI to exclude cuff pathology usually demonstrates denervation muscle oedema in the affected muscles and can prompt and earlier nerve diagnosis. Unfortunately an MRI was not requested in this case despite the normal ultrasound findings.
    In the context of a brachial plexus injury, MRI is valuable to examine the integrity of the nerve roots at the foramen. An MRI scan of the brachial plexus may demonstrate a pseudomeningocoele confirming the presence of a nerve root avulsion. High resolution MRI scan of the cervical spine may demonstrate cord displacement, disruption of the intra-dural ventral and dorsal rootlets, signal change within the cervical spinal cord due to rootlet avulsion and oedema. MRI scan of the brachial plexus may show oedema in root ruptures and loss of nerve continuity, however it cannot assess the quality of the proximal nerve root nor the size of the gap to be reconstructed. MRI scan of the cervical spine in degenerative nerve root compression is important to exclude a neurosurgical target for nerve decompression.
    When nerve transfer surgery is undertaken for degenerative nerve root compression it is important to establish that the rotator cuff is anatomically intact. This patient group is generally older than those patients who sustain high-energy supraclavicular traction brachial plexus injuries. In the older patients with degenerative root compression, loss of the C5 motor function with paralysis of deltoid may unmask a previously undiagnosed rotator cuff tear. Nerve transfer reconstruction of function to the rotator cuff should therefore only be considered in these cases after careful consideration and discussion of the feasibility of subsequent rotator cuff repair with a shoulder specialist. Otherwise attention should be given to deltoid reconstruction through nerve transfer to the axillary nerve and if needed a reverse shoulder replacement can be employed for pain and dysfunction from rotator cuff arthropathy should the grade of deltoid recovery be sufficient to power the arthroplasty.
    Neurophysiological investigations including electromyography are essential components of the preoperative assessment of patients prior to nerve transfer surgery. Electromyography (EMG) can assess the extent of denervation of the potential target muscle as well as the integrity of the function within the donor. In cases of degenerative nerve root compression the window for reconstruction may be longer than the 12 months suggested for complete peripheral nerve lower motor neurone lesions. In a research setting quantitative assessment of the motor unit size using EMG may identify patients suitable for targeted reinnervation beyond the typical 12-month window. Non-functional residual axons in the target nerve may collaterally sprout within the muscle, increasing the motor unit size and providing an auto “babysitting” function, potentially rendering the muscle responsive to new incoming motor axons for longer than complete peripheral nerve injury, extending the window for reconstruction beyond 12 months.
    ALTERNATIVE OPERATIVE TREATMENT
    In the setting of isolated SSN palsy with preservation of some abduction (deltoid) and external rotation (teres minor) functional rehabilitation is the key to a reasonable outcome. If external rotation remains weak then musculo-tendinous transfer of the latissimus dorsi can improve strength but is seldom necessary.
    NON-OPERATIVE MANAGEMENT
    Non-operative treatment strategies include therapy training to improve compensation in intact muscles.
    CONTRAINDICATIONS
    The main contraindication to nerve transfer surgery is a muscle that has been denervated for too long, typically between 9 and 12 months for a lower motor neurone complete injury. Patients must be able to understand the planned treatment and be able to comply with the extensive period of post operative rehabilitation necessary to achieve a functional outcome.

    Setup

    The patient is consented for general anaesthesia exploration and decompression with the option to proceed to autologous nerve graft or nerve transfer.
    The anaesthetist should perform anaesthesia with no neuromuscular paralysis or only using a short-acting paralysis so that intra-operative nerve stimulation may be performed to assess integrity of the SSN.
    The patient is placed in the lateral position with slight forward roll and the operated side uppermost. The torso should be supported with posts posteriorly at the lower lumbar spine and anteriorly at the anterior superior iliac spines. The operated arm should be supported in a gutter. An alternative position is to perform the operation in the prone position. I avoid this position because of a concern regarding traction on the brachial plexus and the added anaesthetic challenges including the need for neuromuscular blockade at induction.
    General anaesthesia is required and either short acting or no neuromuscular paralysis is essential. Intra-operative nerve stimulation is a mandatory requirement for this procedure and successful nerve transfer can only be achieved after confirmation of normal stimulation in the donor nerve and absent stimulation in the recipient.
    I use a regional anaesthesia block needle with stimulation provided by anaesthetic nerve stimulator which provides a range of stimulation from 0.02mA to 5mA at a frequency or 60Hz. The needle is covered with an arthroscopy camera drape and the circulating team activate the stimulator and make the adjustments as requested by the operating team. The patient requires an electrode outside the operative field to complete the circuit.
    During dissection and localisation of nerves a Mixter (90 degree fine pointed clip) is a convenient way of passing tagging and insulating colour-coded surgical rubber sloops around nerves. These rubber sloops allow gentle traction on a nerve for the neurolysis and mobilisation and minimise handling of the epineurium. They provide an insulation against cross stimulation to adjacent nerves when used to lift a nerve during assessment with higher stimulation thresholds.
    An operating microscope should be available. A set of surgical micro-instruments is essential for performing nerve transfer surgery. Neurotomes enable clean nerve transection without crush injury and serrated microsurgical scissors are useful for debriding epineurium. The co-aptation is performed using curved needle holders and 8’0 or 9’0 monofilament non-absorbable suture depending on the diameter of the nerve transfer at the co-aptation site.
    TisseelTM is used as a biological tissue glue (fibrin) to support the co-aptation site and minimise the need for sutures which may distort the nerve ends and create scar at the neurorraphy site.

    Operation – 1

    The patient is positioned in the right lateral position with the left shoulder uppermost. The upper arm is supported on a gutter. The whole limb is exposed and will be prepped including the anterior and posterior aspects of the shoulder, the posterior neck, the back to beyond the midline and inferiorly beyond the tip of the scapula. The arm and hand must be visualised when undertaking nerve stimulation to confirm the nerve anatomy and prevent inadvertent iatrogenous nerve injury. The uppermost leg is shaved and a tourniquet applied to the thigh but not inflated. This limb can be accessed for harvest of a sural nerve graft if needed. The dependent lower limb has TED stockings and a pneumatic Flotron applied for reducing thromboembolic risk. A warm air blanket is used to prevent hypothermia because a large area of torso is exposed.

    The upper leg is shaved and prepared for the small possibility of a sural nerve graft harvest. A thigh tourniquet is applied but not inflated. In this case the late presentation means that a graft is less favourable than a distal nerve transfer. However there are situations where a graft is needed: Poor stimulation of the XIth donor nerve intra-operatively; distal rupture so that the XIth nerve cannot be transferred without a graft.

    The midline is marked by palpation of the spinous processes of the thoracic spine.
    The medial border of the scapula is marked.
    The suprascapular notch and the suprascapular nerve are found 50% of the distance from the medial scapula border to the lateral edge of the acromion. The medial branch of the spinal accessory nerve is 40% of the distance from the midline to the lateral border of the acromion.

    The leg is prepped and draped with a limb pack. The tourniquet hasn’t been inflated. If a nerve graft is required, the leg will be elevated or exsanguinated with an Esmarch bandage. Usually simple elevation is best because there will be incomplete emptying of the short saphenous vein which can be used as a landmark to identify the sural nerve.

    The whole of the upper limb of the operated arm is prepared so that the limb can be observed and palpated during nerve stimulation.

    The limb is prepped and draped and positioned on a gutter. There should be padding in the axilla to prevent compression of the brachial plexus by the proximal edge of the gutter. The dorsal field extends to the midline and beyond the inferior scapula pole. This is important for identification of landmarks because the position of the scapula can change as the arm is moved. The contraction of trapezius must also be visualised during stimulation if a nerve transfer is planned.

    The scapula is marked in the position after preparation of the skin and draping.

    The original landmarks are checked and the position of the notch and the medial branch of the XIth nerve are marked.
    The notch is at the midpoint of the upper border of the scapula 50% of the distance from the medial border to the lateral edge of the acromion.
    The medial branch of the XIth nerve is located 40% of the distance from the midline to the lateral edge of the acromion.

    The final markings prior to skin incision.

    A transverse incision is made superior and parallel to the scapula spine at the level of the upper border of the scapula.

    A cutting diathermy with an epitome circumferential wire cutting blade is used for the initial exposure to the trapezius. The dermis is thick and will bleed considerably. Complete the exposure and insert a self-retaining retractor in the interval. The tension of the skin edges will reduce the bleeding and achieve satisfactory haemostasis.

    The loose areolar tissue is divided to the trapezius muscle using the cutting diathermy.

    The trapezius muscle fibre orientation is noted and a split in the transverse fibres in the line of the incision allows exposure of the supraspinatus. Care should be taken at the medial edge due to the position of the medial ranch of the XIth nerve lying on the undersurface of the trapezius muscle at this point.

    Bipolar diathermy is now used to cauterise vessels within the muscle due to the proximity of the XIth nerve.

    The deep surface of the muscle is exposed with Jamieson scissors and the fat pad over the scapula and the supraspinatus can be seen deep to the trapezius muscle.

    The fascia over the supraspinatus has beed exposed. The medial edge of the trapezius split demonstrates a vessel on the under surface of the muscle. The XIth nerve will be running with this vessel. Care should be taken to avoid injury to this nerve or excess tension with retractor jaws.
    Typically when undertaking a nerve transfer the possible recipient nerve is first exposed and confirmation of the need to proceed with transfer is made prior to exposure and potential injury to the donor. In this situation I tend to identify the donor position and note it or tag it as it is at the edge of the primary exposure surgical field and the deep exposure is challenging requiring muscle retraction and this could pose a risk to the donor nerve if the retractor is mal-positioned.

    Careful medial dissection is performed to identify the position of the XIth nerve.

    The neurovascular bundle is clearly seen deep to trapezius and is demonstrated here with a Langenbeck retractor placed in the medial skin edge.

    Nerve stimulation confirms normal thresholds for trapezius contraction at 0.1mA.

    A 90-degree tipped fine Mixter forceps is useful for mobilising neurovascular bundles and passing sloops around nerves without excessive handling or traction.

    The fascia is incised lateral to the neurovascular bundle and the dissection is completed with Jamieson scissors.

    This fascia is thick and must be fully released prior to nerve and vessel exposure. Care should be taken to avoid cutting any nerve branches traversing this interval and entering the undersurface of the trapezius muscle.

    The fascia is divided to the edge of the neurovascular bundle.

    The medial and lateral edges of the bundle are exposed and a Mixter is passed deep to the medial branch of the XIth nerve (spinal accessory).

    The jaws are gently spread to assist development of the plain. care should be taken when the jaws are closed to prevent grasping the deep surface of the nerve. Turning the Mixter 15 degrees prior to closure helps prevent this.

    Operation – 2

    A blue sloop is introduced flush with the tips of the Mixter jaws to prevent snagging the nerve when the Mixter is withdrawn and the sloop is passed around the nerve.

    Carefully close the Mixter jaws using the rotation technique described earlier.

    The medial branch of the spinal accessory nerve is now isolated in the blue sloop.

    Next the lateral part of the wound is used to expose the suprascapular nerve. Bipolar diathermy is used to coagulate small vessels crossing this interval.

    A laterally place malleable retractor can be used to aid exposure of the supraspinous fossa, the muscle and the upper border of the scapula.
    This is the most challenging part of the operation because the three dimensional anatomy of the suprascapular notch is difficult to appreciate and changes with scapula position.
    My system for identification of the notch includes the following steps:
    Palpate the deep and posterior aspect of the clavicle in the upper and lateral wound
    Deep and distal to the clavicle palpate the coracoid base
    Trace the contour of the bone from the coracoid base along the upper border of the scapula in a medial direction
    The ligament is medial to the coracoid base and may be ossified
    The omohyoid muscle inserts on the ligament and can be visualised
    The suprascapular artery lies in the fat superficial to the ligament
    The supraspinatus muscle and fascia lies distal to the ligament and can be palpated
    Sloop the artery and retract medially
    Divide the omohyoid or elevate the insertion with a periosteal elevator
    Dissection the fat proximal to the ligament using scissors opened in an oblique direction aimed towards the ipsilateral scapula inferior pole
    The nerve is identified proximal to the fascia and can be protected with a sloop
    In a case of rupture the proximal SSN may not be identified easily and therefore I would recommend if the SSN is not seen that the surgeon tries an exposure of the supraspinatus muscle distal to the upper border of the scapula and identify the nerve in the supra-spinous fossa and trace superiorly.

    The supraspinatus muscle is exposed.

    The suprascapular artery can be seen proximal to the supraspiantus muscle and this passes distally superficial to the suprascapular ligament.

    Medium ligaclips are applied to the side branches of the suprascapular artery and to the venae commitantes before division. Traction ofn these vessels can tear them resulting in bleeding that is difficult to control and risks diathermy injury to the suprascapular nerve beneath.

    A second ligaclip is applied.

    The branch is divided to allow the suprascapular artery to be mobilised.

    A Watson-Cheyne can be used to palpate the suprascapular notch and the overlying ligament. The SSN passes deep to the ligament and is difficult to see because the ligament maintains its position deep in the wound. The position of the nerve will become obvious when the ligament is released. The Watson-Cheyne is positioned with its tip alon the inferior edge of the suprascapular ligament.

    The ligament is carefully released and then the SSN naturally mobilises superficially in the wound through the notch. The SSN is seen passing to the notch and a Mixter and yellow sloop can be used to tag the nerve for identification and gentle retraction.

    The sloop is carefully delivered around the SSN avoiding traction or snagging on the deep surface.

    The sloop delivered around the SSN.

    Stimulation to 5.0mA demonstrates no function in the nerve prior to decompression.

    The SSN can be traced distally towards the supraspinatus beyond the notch.

    The nerve is retracted and is seen to branch into the supraspinous fossa after external neurolysis and release of fascial bands at the distal edge of the resected ligament.
    This confirms that there is no distal neuroma or rupture of the SSN.
    Without a rupture or a neuroma to graft the regenerative capacity of the SSN is uncertain. There is no recovery at 10 months. There is no option to come back for a nerve transfer should this decompression not recover and so the decision is made at this point to proceed to a nerve transfer as being the most reliable reconstructive option at this time post injury.

    The second blue sloop is around the main SSN. The left yellow sloop is around the branch to supraspiantus and the right yellow sloop is around the infraspinous branch of the SSN that will traverse the spinoglenoid notch under the spinoglenoid ligament to the infraspinatus. A nerve stimulator is used to assess the nerve at all three positions to exclude a conduction block at the level of the notch. In this case there was no stimulation proximally on the SSN or on either of the 2 main branches distal to the notch.

    The other identification sloops are removed and in this case the yellow sloop has been replaced around the main SSN. The yellow sloop will be the nerve transfer recipient and the XIth nerve in the blue sloop will be the transfer donor.
    Proximal external neurolysis of the SSN is required to confirm that there is no neuroma and to achieve sufficient length for the transfer and a tension-free co-aptation without an interposition graft.
    The distal medial branch of the XIth nerve is neurolysed to gain sufficient length for direct transfer to the SSN. The XIth nerve is sectioned distally.

    Normal stimulation of the spinal accessory nerve is confirmed prior to sectioning distally for transfer. The nerve branches and the branches may limit the rotation of the nerve for transfer if spared. If taken they should all be of sufficient length so that they can be included in a single co-aptation site. Sometimes with inter-branch neurolysis it is possible to maintain a significant XIth medial branch and still rotate a branch of sufficient size for the transfer. How this part of the procedure is performed depends of the individual branching anatomy and the preference of the surgeon.

    Microsurgical background has been placed under the proximally sectioned SSN to aid visualisation and reduce blood clots impacting on the microsurgical instrumentation. There is plenty of length here and the distal stump can be trimmed when the donor is rotated into position if there is sufficient length. This would bring the co-aptation closer to the denervated muscle and reduce the time for reinnervation. It should be not trimmed if it creates tension.

    The XIth medial branch is sectioned distally for transfer.
    REMEMBER: “Donor distal and recipient proximal” when undertaking the neurotomies.
    I use scissors at this point but neurotomes can be used if access is not a problem or later to trim the nerve end prior to co-aptation and ensure fresh clean nerve ends.

    Proximal neurolysis of the XIth nerve should be completed prior to the neurotomy to avoid excess handing of the nerve for transfer. The position is being checked here as there is a residual proximal tether point.

    The donor and recipient nerves are positioned ready for the operating microscope to be brought in to position for the co-aptation.

    There is a good size match and the co-aptation will be possible without tension.

    Operation – 3

    The microscope is used for the co-aptation with 9’0 nylon interrupted sutures. Between 2 and 4 sutures are typically used for alignment without distortion of the nerve end s at the co-aptation site.

    The nerve co-aptation in progress.

    In this case 3 sutures are placed at 120 degree intervals.

    The undersurface of the completed neurorraphy demonstrates excellent alignment and no distortion or tension.

    The completed neurorraphy ready for TisseelTM fibrin glue augmentation.

    TisseelTM fibrin glue is supplied frozen and should be defrosted to 37 degrees centigrade. There are 2 syringes: One contains fibrinogen and one thrombin. The fluids are mixed at the tip of a specially designed double barrelled nozzle and applicator. Between uses the fibrin clot blocks the nozzle tip and spare ones are available for tip exchange between uses if several applications are required in one patient.
    The TisseelTM activates and form fibrin clot within a few seconds if at the correct temperature.

    The background material is removed and the nerve transfer is supported with additional TisseelTM applied to the surgical bed.

    The completed transfer prior to wound closure.

    The trapezius muscle split is closed over the transfer.

    The fascia is closed with vicryl 2’0 sutures.

    The subcutaneous tissues are opposed with interrupted 3’0 vicryl sutures.

    Completion of the subcutaneous tissue closure.

    The skin is closed with a continuous subcuticular monofilament absorbable monacril 3’0 suture.

    Completing the subcuticular closure.

    The knots are buried.
    Long acting local anaesthetic is infiltrated to the wound edges.

    Steristrips are applied to support the wound edges.

    A dressing is applied to the wound.
    The arm is placed in a polysling with a body strap to prevent inadvertent traction on the nerve transfer during recovery from the anaesthetic and for support for three weeks post-operatively.

    Post Operative

    A waterproof dressing with absorbent pad is applied to the wound. The wound should be kept clean and dry for 7 days after which the patient can shower then replace the dressing. A polysling is applied to the upper limb with a torso strap around the waist before the patient wakes from surgery. The polysling and torso strap should be maintained for 3 weeks to prevent excessive passive movement at the shoulder.
    During this phase the patient is encouraged to maintain isometric contraction of the donor muscle in the sling and to visualise the combination of trapezius activation and shoulder abduction and external rotation.
    Nerve transfer rehabilitation involves a 6-phase programme of activity developed at the Centre for Nerve Injury and Paralysis, Birmingham, UK.
    Phase 1 – Pre-operative phase: Education and donor optimisation. Introduction to trophic stimulation and the concept for functional electrical stimulation (FES).
    Phase 2 – Protection phase: During the immediate post-operative period the nerve transfer is protected from inadvertent injury with the arm immobilised. Isometric contraction of the donor and visualisation of the combination donor-recipient action is performed during this period which typically lasts 3 weeks.
    Phase 3 – Prevention phase: During this phase the arm is mobilised and neural gliding is commenced. Joint range of motion exercises (active and passive) are commenced to prevent joint contractures developing. The isometric exercises are continued and isotonic and eccentric exercises are commenced for the donor muscle to maintain function and restore strength. Functional stimulation can be commenced on the donor muscle. Trophic stimulation can be maintained on the recipient muscle.
    Phase 4 – Power phase: During this period the donor muscle is strengthened and the recipient muscle starts to respond. Typically the first sign of reinnervation is a tender muscle squeeze sign due to small fibre reinnervation. Typically this is 3 months following transfer but is affected by the distance of the co-aptation from the recipient motor point.Visible flickers of contraction follow within 6 weeks and donor activation potentiate the recipient response. FES continues and the phase lasts for approximately 6-12 months during which useful motor grade returns: Medical Research Council – (MRC) Grade 3-4.
    Phase 5 – Plasticity: During this phase the patient works on activation of the recipient muscle without activation of the donor. This phase can overlap with phase 4 and is guided by a therapist specialised in nerve transfer rehabilitation.
    Phase 6 – Purpose: During this phase the patient introduces function tasks discussed as objectives during the pre-operative phase. This period of training is tailored to the individual and includes work hardening. Improvements are typically found in power and functional performance for at least 2 years following nerve transfer surgery.

    Recommended Reading

    The technique of transfer of the XIth nerve to the SSN is not new. Critical appraisal of the results of an anterior transfer using the lateral branch demonstrate reasonable shoulder abduction but relatively poor external rotation in brachial plexus injuries with total loss of C5 function. In such situations I prefer 2 transfers for abduction and 2 transfers for external rotation (posterior approach XI medial branch to SSN; Triceps medial head branch to axillary nerve). This technique reinnervates supraspinatus, infraspinatus, deltoid and teres minor. Useful (strong MRC grade 4) function can be achieved in the majority of cases if patient selection guidelines are adhered to as discussed earlier in this review. This approach is supported in the literature with a double nerve transfer achieving improved shoulder abduction MRC Grade 4 in 74% compared to 35% with a single nerve transfer and 46% of grafts alone. There is bias as the grafts are only possible in ruptures of the upper trunk and the injury patterns may be different. The range of external rotation was also greater with a double nerve transfer in this series by Wolfe et al. in 2011. Papp et al. define the need for distal decompression after proximal nerve injury in their paper from 1998.
    This technique is for an isolated SSN palsy and the posterior approach allows transfer close to the denervated muscle allowing rapid reinnervation despite the late diagnosis and referral in this case.
    the additional benefits of the posterior approach include no denervation of the lateral trapezius which is also a shoulder elevator and the opportunity to identify a neuroma or rupture at the notch in trauma that would otherwise not be seen through the anterior approach. These concomitant injuries may explain the poorer results when transfer is undertaken anteriorly using the lateral branch of the XIth nerve. The posterior approach is technically more demanding and the anatomy of the suprascapular notch is difficult to appreciate. Using the steps I describe to assist in localisation of the notch and the SSN will help the occasional surgeon.
    References:
    Garg R, Merrell GA, Hillstrom HJ, Wolfe SW. Comparison of nerve transfers and nerve grafting for traumatic upper plexus palsy: a systematic review and analysis. J Bone Joint Surg Am 2011 May 4;93(9):819-29. doi: 10.2106/JBJS.I.01602.
    Leechavengvongs S, Malungpaishorpe K, Uerpairojkit C, Ng Cy, Witoonchart K. Nerve transfers to restore shoulder function. Hand Clin 2016 May;32(2):153-64. doi: 10.1016/j.hcl.2015.12.004.
    Yang LJ, Chang KW, Chung KC. A systematic review of nerve transfer and nerve repair for the treatment of adult upper brachial plexus injury. Neurosurg 2012 Aug;71(2):417-29; discussion 429. doi: 10.1227/NEU.0b013e318257be98.
    Schoeller T, Otto A, Wechselberger G, Pommer B, Papp C. Distal nerve entrapment following nerve repair. Br J Plast Surg 1998 Apr;51(3):227-9; discussion 230.

    Reference

    • orthoracle.com

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