The orthopedic surgeon is often the first to correctly identify a nerve problem related to the shoulder. Patients may have a chief complaint of shoulder pain that in fact is a manifestation of a neurologic condition. Patients with shoulder injuries not infrequently have concomitant neurologic conditions. In addition, orthopedic surgery is the most common cause of iatrogenic peripheral nerve injury requiring treatment. Knowledge of the common nerve lesions in the shoulder region allows the surgeon to recognize these entities in the clinic setting, and knowledge of the relevant neural anatomy will help surgeons to avoid potential nerve injury in the operating room. Recent advances in diagnostic studies, nerve repair and reconstruction techniques, and novel tendon transfers have improved our ability to identify and treat patients with nerve-related disorders about the shoulder.
Clinical evalution
Patients with nerve injuries are often evaluated following significant trauma. Commonly, the patient is confused, incoherent, sedated, or even unconscious, and it can be difficult to perform a satisfactory neurologic examination before initiating surgical care. Nonetheless, a good neurologic examination should be attempted in the emergency department. If for any reason an adequate examination cannot be performed, this should be noted in the patient’s medical record. Specifically, if the function of a particular nerve cannot be properly assessed preoperatively, the record should include such information. Too often in the emergency setting, the patient receives only a cursory evaluation, and perhaps the most junior person on the orthopedic surgical team writes in the clinical record that the extremity was “neurovascularly intact.” These two words, if inaccurate, are sometimes the origin of unnecessary litigation. Such general terms should not be used when recording a patient’s examination; instead, individual muscle strength, sensory examination, and deep tendon reflexes should be carefully documented in the patient’s record.
A detailed neurologic evaluation of the upper extremity can be performed on a coherent patient in a relatively short amount of time, even if the patient has a shoulder dislocation or proximal humerus fracture. It is often easiest to start at the hand and progress proximally during the examination. Radial, median, and ulnar nerve function can all be assessed by a thorough evaluation of the hand and wrist, which should take less than a minute. Elbow flexion and extension strength are relatively simple to determine. However, the examiner should be aware that it is possible to flex the elbow strongly with the action of the brachioradialis without having any function of the biceps. Loss of motor or sensory function in the distal end of the extremity can help to direct examination of the more proximal musculature. For example, loss of radial nerve function should make the examiner look closely at axillary nerve function because both nerves are derived from the posterior cord. Likewise, loss of median nerve function might also affect the musculocutaneous nerve if the lesion is in the lateral cord.
Progressing up the arm, the condition of the medial and lateral pectoral nerves can be assessed by individually testing the strength of each of the major portions of the pectoralis major. The deltoid and rotator cuff muscles are then examined. The deltoid can be assessed even in the case of a painful proximal humeral fracture or glenohumeral dislocation. With the arm at the side, the patient is instructed to push out or “elbow” the examiner’s hand (which is placed at the lateral aspect of the elbow, with the other hand over the deltoid region to feel for contracture). If the patient is in a great deal of pain and the examiner cannot adequately determine the condition of the axillary nerve, this information should be recorded in the clinical record. Do not assume that it “might be okay.”
Examining shoulder abduction is an important part of the examination, both to record muscle strength and to visualize shoulder kinesis through the arc of motion. Two important points are relevant here. First, some patients are able to abduct the shoulder through a full arc of motion by using either just the supraspinatus or the deltoid in the face of complete paralysis of either of them. Ensuring muscle contraction is a critical element in this part of the examination. Second, visualizing and palpating the scapula are necessary parts of the examination, especially when there is possible dysfunction. For example, patients with winged scapulae due to weakness of the serratus anterior or trapezius may have difficulty abducting the arm fully without the scapula stabilized and may compensate with trick motions. The examiner should recognize the clinical appearances and know the techniques to examine winging of the scapula, particularly with respect to distinguishing serratus anterior, trapezius, and rhomboid muscle dysfunction. In addition, a useful test for serratus anterior function that can be applied even in a patient with complete brachial plexus lesion is to stabilize the inferior pole of the scapula while the patient pushes the arm forward; patients unable to perform this test would not be able to perform the more standard push-off test with the arms extended against a wall.
The examiner needs to evaluate the patient for other conditions besides a neurologic etiology that can cause lack of movement. In particular, it should be considered whether the inability of a patient to externally rotate the arm or perform the lift-off test might represent a neurologic lesion affecting the infraspinatus or subscapularis, a rotator cuff tear, or both. A patient who is feigning paralysis in the upper limb for secondary gain issues cannot voluntarily stop the latissimus dorsi from contracting while coughing.
Proper examination of the shoulder begins well above the shoulder, even above the neck, and continues on through the distal portion of the limb. Proximal and distal lesions should always be considered when examining a patient with shoulder pain or weakness and establishing a differential diagnosis. Cervical radiculopathy is a common cause of pain in the shoulder accompanied by motor weakness and sensory loss in the upper extremity. In this situation, flexion and extension of the cervical spine, or Spurling maneuver, might reproduce or exacerbate the patient’s symptoms. Upper motor neuron lesions can also result in shoulder weakness. In these cases, the deep tendon reflexes may be hyperreflexic, pathologic reflexes may be present, and tone may be increased. The clinical examination should exclude referred pain as a possibility because cardiac, intrathoracic, and intra-abdominal complaints may manifest as shoulder pain.
Finally, examination of the shoulder should always be performed with both shoulders exposed. Visualization is the first component of a physical examination, but this step is often neglected because of time constraints or modesty issues. If the bare scapula is not examined, it is easy to miss atrophy of the spinatus muscles. Bilateral atrophy or weakness would certainly change the differential diagnosis and force the examiner to consider an underlying neurogenic or myopathic condition.
Musculocutaneous nerve
Anatomy
The musculocutaneous nerve originates from the lateral cord of the brachial plexus, provides motor innervation to primarily elbow flexors, and terminates as the sensory lateral antebrachial cutaneous nerve. It travels obliquely inferior to the coracoid process and traverses through the coracobrachialis muscle. The main trunk of the musculocutaneous nerve enters the muscle approximately 5 cm from coracoid and exits 7.5 cm distal. , However, in nearly 30% of patients, the nerve enters the coracobrachialis proximal to 5 cm from the coracoid, and small branches of the nerve can be found inserting into the coracobrachialis as close as 1.7 cm below the coracoid. The nerve travels between the brachialis and biceps muscle before piercing the biceps muscle approximately 11.5 cm distal to the coracoid. Finally, the nerve pierces the fascia lateral to the biceps tendon, where it continues on to provide sensation to the lateral forearm.
Patients with musculocutaneous neuropathy typically present with complaints of pain and sensory deficits. In a small percentage of patients, isolated lateral antebrachial cutaneous dysfunction may be seen. However, the majority will have some electrodiagnostic evidence of motor involvement. Interestingly, patients may not demonstrate weakness clinically.
Etiology
The musculocutaneous nerve is most commonly injured in association with a severe brachial plexus injury (BPI). Isolated musculocutaneous nerve injury is rare due to its relatively short course deep in the proximal arm. In a series of patients diagnosed with isolated musculocutaneous neuropathy, the etiology was trauma in 43% and iatrogenic in 22% of individuals. As an isolated traumatic injury, penetrating trauma is the most common cause. However, reports of isolated musculocutaneous neuropathy have been reported following glenohumeral dislocation , and even strenuous activity.
Iatrogenic injury to the musculocutaneous nerve has been reported following the Bristow procedure, coracoid process transfer for clavicle instability, and subpectoral biceps tenodesis. It is important for operating surgeons to recognize the importance of maintaining the origins of the coracobrachialis and short head of biceps. When these muscles are allowed to remain on the coracoid during surgery, they act as a tether to overzealous retraction. In fact, exposure of the posterior cord or the axillary nerve can lead to musculocutaneous nerve palsy as a result of retraction. Therefore care must be taken to avoid excessive traction on the musculocutaneous nerve during dissection. Alternatively, detachment of the conjoined tendon allows excellent exposure and potentially decreased pressure on the entire brachial plexus. Actual detachment of these muscles from the coracoid and reattachment to the anterior glenoid relaxes the musculocutaneous nerve. Still, the surgical manipulation required for this procedure may result in damage to the nerve.
Iatrogenic injury during arthroscopic procedures is far less common. Iatrogenic injury to the musculocutaneous nerve may be due to patient positioning and traction or traction in the lateral decubitus position. Anterior portals that stray medial to the coracoid put the musculocutaneous nerve and other branches of the brachial plexus at risk for injury. With the low anterior 5 o’clock portal during arthroscopic shoulder surgery, instruments travel within 10 mm of the musculocutaneous nerve. In their review of iatrogenic nerve injuries following shoulder surgery, Carofino and colleagues identified seven patients in whom the musculocutaneous nerve was affected. Two resulted from open procedures, three from arthroscopic procedures, and two from combined arthroscopic and open procedures.
Nonoperative treatment
If the musculocutaneous nerve is noted to be sharply transected during a surgical procedure, it may be amenable to immediate primary repair. However, the majority of patients seen after trauma or surgery with an injury to the musculocutaneous nerve should be observed initially. If no improvement in function is noted, an electromyography and nerve conduction study should be performed at 3 to 4 weeks. Most postoperative musculocutaneous neuropathies are traction injuries that resolve over a period of weeks to months, depending on the extent of the injury.
Operative treatment
In general, surgical options following injury to the musculocutaneous nerve include neurolysis, neuroma resection and nerve grafting, nerve transfers, and tendon transfers. Ideally, surgical exploration should be taken if no improvement in biceps and brachialis function is noted on clinical examination or serial electrodiagnostic studies by 6 months from injury. If the nerve appears intact at the time of surgical exploration but is compressed by scar tissue and demonstrates electrical conduction across the lesion, neurolysis may be performed. If surgical exploration reveals a neuroma in continuity that does not conduct a nerve action potential (NAP) or reveals a rupture or transection of the nerve, neuroma excision with nerve grafting is preferred.
Nerve transfers have increased in popularity over the past two decades for the treatment of brachial plexus and peripheral nerve injuries. These shorten the time to innervation and bypass the need to dissect in scarred or previously traumatized soft tissue. Oberlin’s technique of transferring a fascicle of the ulnar nerve directly to the motor branch of the biceps muscle is one of the most common and best studied of these transfers. A so-called double Oberlin transfer uses fascicles of the median and ulnar nerve to innervate the brachialis and biceps muscles, respectively. , With these nerve transfers, reinnervation in the biceps may be seen approximately 3 months following the procedure. The reduced time to reinnervation is due to a shorter distance from the nerve transfer to the target muscle compared with more proximal nerve repair or reconstruction. In addition, antigravity elbow flexion is reliably restored in 90% of patients with either technique. However, a recent systematic review found that more patients achieved M4 or greater strength following double nerve transfers compared with single fascicular nerve transfer for restoration of elbow flexion.
If patients are seen more than 1 year after musculocutaneous nerve injury, nerve repair or reconstruction is significantly less likely to be successful. Some patients with little or no biceps or brachialis function may still be able to actively flex their elbow using brachioradialis alone. For those with insufficient elbow flexion strength, a variety of tendon transfers have been described. Popular options include Steindler flexorplasty (proximal advancement of the flexor-pronator muscle group) as well as triceps, pectoralis major, pectoralis minor, and latissimus dorsi transfer. Free muscle transfer is also a possibility in patients in whom these potential donor muscles are not available.
Axillary nerve
Anatomy
The axillary nerve originates from the posterior cord of the brachial plexus, provides motor innervation to the deltoid and teres minor muscles, and terminates as the sensory superior lateral brachial cutaneous nerve. The axillary nerve runs lateral to the radial nerve, posterior to the axillary artery, and anterior to the subscapularis muscle. The nerve may be located during an anterior approach by sweeping an index finger inferiorly over the anterior subscapularis and gently hooking the nerve while simultaneously palpating it on the underside of the deltoid with the other index finger. The nerve enters the quadrilateral space with the posterior humeral circumflex artery and is in close proximity to the inferior shoulder capsule. As it exits the space, the axillary nerve continues to the posterior aspect of the humeral neck and divides into anterior and posterior branches. The posterior branch of the axillary nerve innervates the teres minor and posterior portion of the deltoid before terminating as the superior lateral brachial cutaneous nerve. The anterior branch passes anterior to the humerus and innervates the deltoid muscle. The position of the anterior branch is commonly reported as lying 4 to 7 cm inferior to the anterolateral corner of the acromion. However, it may be found as close as 3.1 cm, and abduction of the shoulder brings the nerve closer to the acromion.
Patients with axillary neuropathy may present with numbness over the lateral aspect of the shoulder. Deltoid weakness may be difficult to appreciate on exam in patients with an intact supraspinatus tendon and those with commonly associated injuries such as anterior shoulder dislocation or proximal humerus fracture.
Etiology
The majority of axillary nerve injuries occur as part of a combined BPI. Isolated axillary nerve injury occurs in only 0.3% to 6% of BPIs. Injury to the axillary nerve most often follows closed trauma involving traction on the shoulder. Axillary nerve paralysis is the most common neurologic complication of shoulder dislocations. Some patients with a proximal humeral fracture or shoulder dislocation have a subclinical axillary nerve lesion that is evident by electromyography/nerve conduction study but which is not apparent clinically. The vast majority of these patients recover from the nerve injury as they rehabilitate from the dislocation or fracture. Blunt trauma to the anterolateral aspect of the shoulder has also been noted to cause injury to the axillary nerve as it travels on the deep surface of the deltoid muscle.
The axillary nerve injury is the most common neuropathy seen among iatrogenic injuries following shoulder surgery. Neuropathy has been reported following both open and arthroscopic procedures, particularly those performed for instability. Yoo et al. found that the axillary nerve lies approximately 10 to 25 mm from the inferior glenoid rim ( Fig. 58.1 ). Thermal capsular shrinkage created a local increase in temperature in the inferior capsule that led to nerve injury in 1% to 2% of patients, and this procedure is currently less commonly performed. Because the nerve is in close proximity to the anteroinferior capsule, the axillary nerve is at risk during arthroscopic Bankart repairs with inadvertent suture placement. Similarly, axillary nerve injury has been reported following capsular resection for adhesive capsulitis. Although less commonly associated with total shoulder arthroplasty, care should be taken with dissection and retractor placement. Injuries to the upper trunk of the brachial plexus have been reported following arthroplasty, which lead to limitations in abduction and forward flexion.
Quadrilateral space syndrome is a rare condition in which compression of the axillary nerve and posterior circumflex humeral artery leads to shoulder pain, swelling, tenderness posteriorly over the quadrilateral space, paralysis, and variable loss of sensation. However, in some cases, the clinical exam may be relatively normal, and electrodiagnostic studies are usually normal. Compression can be caused by fibrous bands in the quadrilateral space, surgical adhesions, paralabral cysts, muscle hypertrophy, or scapular fractures. Magnetic resonance imaging (MRI) may be helpful in identifying changes in the deltoid or teres minor muscles and any fibrous bands that may benefit from decompression.
Nonoperative treatment
Young patients may be able to compensate for complete deltoid paralysis and can often perform activities of daily living with only partial disability. The shoulder can easily maintain full range of motion with an intact rotator cuff. However, most patients experience early fatigue in the involved side with repetitive activities. Although deltoid atrophy is quite evident in a fit person, it can sometimes be difficult for the examiner to detect deltoid atrophy in a fit patient. Injury to the sensory superior lateral cutaneous nerve of the arm can lead to loss of sensation over the lateral aspect of the shoulder. However, the diagnosis of axillary neuropathy should not be determined by the presence or absence of lateral shoulder sensation. The sensory nerve may be spared from injury, or overlapping sensory innervation from other cutaneous nerves may mask the nerve deficit.
Patients with a history of blunt trauma to the axillary nerve should be observed over at least a 3-month period before operative treatment is considered. Without clinical improvement, a baseline electrodiagnostic study should be performed at 3 to 4 weeks following injury. Physical therapy emphasizing active and passive exercises should be initiated to preserve range of motion and prevent joint contracture until strength recovers. Most patients progress to full recovery following injury. , ,
Observation is the usual treatment for quadrilateral space syndrome, and the vast majority of patients will improve with time. Surgical exploration of the quadrilateral space and release of scar or fibrous bands may be effective in patients refractory to nonoperative treatment. ,
Operative treatment
Rarely does injury to the axillary nerve warrant early operative treatment. However, in sharp, penetrating injuries or in cases where an iatrogenic nerve injury is identified at the time of surgery, it may be amenable to primary repair.
For patients initially treated with observation but without clinical or electrodiagnostic evidence of recovery by 4 to 6 months, surgical exploration is warranted. Intraoperative neuromonitoring is invaluable in evaluating nerve lesions in continuity. The presence or absence of NAPs helps to decide whether to perform neurolysis or neuroma resection. In select cases, good results with neurolysis have been demonstrated. , The axillary nerve travels a relatively short distance from its origin off the posterior cord to the deltoid motor endplate. This may make neurolysis difficult but also coaptation following neuroma resection. Thus repair of the axillary nerve is commonly performed with cabled sural nerve graft when neuroma excision is necessary.
Nerve transfers from the medial pectoral, thoracodorsal, spinal accessory, phrenic, and branches of the radial nerves and intercostal nerves have all been described in cases where direct repair or cable grafting of the axillary nerve itself is not possible. Leechavengvongs described a nerve transfer using a triceps branch to the anterior division of the axillary nerve in patients with upper trunk brachial plexopathy. However, in a series of patients with isolated axillary nerve injury treated with this nerve transfer, 24% of patients failed to achieve more than M3 strength. Worse outcomes were observed in patients with delays in treatment and those older than 50 years of age.
Patients seen more than 12 months after injury usually do not benefit from surgical repair of the nerve because of loss of deltoid muscle motor endplates. In patients with poor shoulder function that limits their activities of daily living but a normal rotator cuff, tendon transfer procedures can be considered. Pedicled pectoralis muscle transfer can be performed to reconstruct the anterior deltoid ( Fig. 58.2 ). The clavicular head of the pectoralis major alone, or the upper two-thirds, or the full pectoralis can be transferred to reconstruct the deltoid, mostly the anterior part. Another option is the transfer of the pedicled latissimus dorsi based on the thoracodorsal neurovascular bundle to reconstruct the anterior deltoid ( Fig. 58.3 ). These transfers could be performed either in isolation or combined with reverse shoulder arthroplasty (RSA). The senior author (B.T.E.) reported on the outcome of pedicled transfer. Thirty-one patients, with an average age of 51 years (range, 27 to 73 years) were included. The patients’ pathology was mostly chronic deltoid paralysis associated with rotator cuff deficiency and progressive arthritis. All patients underwent RSA with pedicled transfer of the upper two-thirds of the pectoralis major to reconstruct the anterior deltoid. Additional transfers for shoulder external rotation included the lower trapezius transfer to infraspinatus in three patients and latissimus dorsi transfer to the infraspinatus insertion in five patients. At an average follow-up of 37 months, 29 patients reported significant improvement of motion and pain. In addition, these patients showed on examination significant improvement in disabilities of the arm, shoulder, and hand, and shoulder range of motion.
Alternatively, to reconstruct middle deltoid function, the upper/middle trapezius can be transferred to the proximal humerus. Different techniques have been described for this transfer, including transfer of the muscle on top of the acromion, lengthened with Achilles tendon allograft, or transfer of the acromial body insertion to the proximal humerus. The outcome of this transfer has been very marginal, especially in patients with no rotator cuff function. We favor pedicled muscle transfers, as described earlier, when these are available, because of the more predictable improvement in shoulder function.
Spinal accessory nerve
Anatomy
The spinal accessory nerve is a cranial nerve XI that exits the skull with the glossopharyngeal and vagus nerves and innervates the sternocleidomastoid and trapezius muscles. It initially descends along the internal carotid artery to pass through the upper portion of the sternocleidomastoid muscle. It then crosses the posterior cervical triangle, which is bordered anteriorly by the sternocleidomastoid muscle, posteriorly by the trapezius, and inferiorly by the clavicle. The nerve lies on the floor of the posterior triangle with only the overlying fascia as protection against injury. It abuts the posterior cervical lymph nodes. The nerve enters the anterior surface of the trapezius and travels inferiorly, parallel to the medial border of the scapula.
Etiology
Injury to the spinal accessory nerve can occur after penetrating trauma to the shoulder. Blunt trauma can also cause loss of trapezius function. However, it is most commonly injured in cervical lymph node dissection or radical neck dissection in the posterior triangle of the neck.
Although iatrogenic injury to the spinal accessory nerve is a rare complication of orthopedic surgery, the orthopedic surgeon may be the first to correctly identify the injury and diagnosis. Patients usually have vague shoulder pain as their primary complaint, and loss of motion may be a secondary concern. The trapezius muscle receives some innervation from the upper cervical nerve roots, and thus there may only be slight visible wasting of the muscle. A high index of suspicion with specific muscle strength testing may help to prevent attributing this injury to postoperative pain or rotator cuff pathology.
The lateral portion of the trapezius is critical in supporting abduction of the shoulder and is innervated exclusively by the spinal accessory nerve. Usually, a shoulder shrug produces the deformity. However, a strong levator scapula can compensate well, and only minimal deformity may be observed. Winging of the scapula often occurs but is subtler than is seen in long thoracic nerve palsy. The shoulder may hang lower or droop in comparison with the contralateral side, which may even cause symptoms of thoracic outlet syndrome. If the patient is carefully observed, the scapula appears to be rotated forward at the shoulder.
Some of the pain that patients experience may be due to strain of other parascapular muscles as they attempt to compensate for the lack of trapezius function. Furthermore, because the scapula cannot properly rotate the acromion away from the humerus as the arm is elevated, impingement of the rotator cuff can cause secondary rotator cuff tendinopathy. Finally, injury to the spinal accessory nerve may produce neuropathic pain. Examination should also include evaluation of possible concomitant injury to other neighboring nerves, such as the cervical plexus or great auricular nerve.
Nonoperative treatment
If more than 12 to 18 months have passed since injury to the spinal accessory nerve and the patient has compensated reasonably well, nonoperative treatment may be considered. The degree of disability varies from patient to patient, even with aggressive physical therapy. Some patients experience only a persistent ache in the shoulder, whereas others feel and act completely disabled with respect to the upper extremity. Braces have been advocated as adjunctive treatment, but they are bulky and not used consistently by patients. A patient symptomatic enough to attempt to use a brace is potentially a candidate for surgical reconstruction.
Operative treatment
Ideally, surgical exploration of the nerve should be performed within 6 months. Although surgical reconstruction of the nerve may be considered 1 year after injury, better results occur with treatment as soon after injury as possible. In cases with a high index of suspicion for nerve injury, especially when the nerve was not identified and protected as part of an operation, we favor immediate exploration of these nerve injuries when they occur.
In this setting, surgical options include neurolysis, direct repair, or neuroma excision and nerve grafting, depending on the intraoperative observations and electrodiagnostic testing. During surgical reconstruction, it is important to consider the acromion-mastoid distance in the anesthetized patient. If direct repair to the nerve is performed with the head tilted toward the operated shoulder, significant traction can occur when the patient is awakened after surgery and transported to the recovery room, and this can disrupt the repair. If the nerve ends are found to have retracted at surgery, it is best to use an interpositional graft, such as sural nerve, to reduce tension on the repair. Alternatively, nerve transfers have been described from the lateral pectoral nerve and the posterior division of the upper trunk to the spinal accessory nerve. , In a series of 11 patients with trapezius palsy following iatrogenic injury to the spinal accessory nerve treated with nerve transfer, 10 patients achieved M4 or greater strength and an average 57 degrees of improvement in shoulder abduction.
Modern surgical procedures currently involve dynamic muscle transfer techniques. However, earlier historical procedures initially involved mostly static repairs. Henry advocated for static stabilization of the medial aspect of the scapula to the vertebral spine with strips of fascia lata. Dewar and Harris described lateral transfer of the levator scapulae to the lateral part of the scapula, combined with a static fascial sling from the vertebral spine to the medial part of the scapula. However, static repairs with fascia, tendon, or artificial materials tend to stretch out or rupture over time.
Dynamic transfer of the levator scapulae along with the rhomboid major and rhomboid minor was described in Germany by Eden and Lange. Bigliani reported good results with this technique.
Elhassan and Wagner proposed a modification of the Eden-Lange (EL) procedure, called the “triple transfer,” with good to excellent results in 22 patients. The authors reported that the line of pull of the rhomboid major and minor, when transferred to the body of the scapula, worked in almost the opposite direction to lower the trapezius, and for this reason, these muscles should independently be transferred more proximally for better replication of the line of pull of the middle and lower trapezius. The triple transfer was subsequently shown in a biomechanical study to better mimic the normal function of the trapezius compared with the traditional transfer. The senior author has performed more than 60 triple transfer for symptomatic chronic trapezius with good to excellent results in 91% of the patients.
The surgical approaches for the EL procedure and the Elhassan-Wagner (EW) modified transfer are similar and involve an inverted L-incision with a vertical incision placed midway between the vertebral spina and the medial edge of the scapula and a horizontal incision extended laterally to the midaspect of the supraspinatus fossa. The atrophied trapezius is detached from the spine of the scapula and acromion and can be used to cover the muscles transferred at the end of the case. If the EL procedure is performed, then the levator scapulae is detached with a small bony insertion, and the rhomboid minor and major are detached together with their small bony insertions. This release can be accomplished with a small saw or an osteotome. At this time, the spine of the scapula is debrided to prepare it for the bony insertion of the muscle transfers. With the EL procedure ( Fig. 58.4 ), the levator scapulae is inserted on the spine of the scapula, posterior to the acromion. The levator should be placed as far laterally as possible on the spine of the scapula, usually 5 to 7 cm medial to the posterolateral edge of the acromion. The rhomboid major and minor can be elevated individually or together from the medial edge of the scapula. The dorsal scapular nerve is potentially at risk during this part of the procedure. The infraspinatus is partially elevated from the scapula in a medial-to-lateral direction. The rhomboids are then placed as far laterally as possible (at least 4 cm) on the posterior aspect of the scapula and secured in place via suture and drill holes through the scapula. Alternatively, the rhomboid minor can be transferred cephalad to the spine of the scapula into the supraspinatus fossa. The infraspinatus is then sutured back in position over the transferred rhomboids.
With the EW transfer, the levator scapulae is placed as lateral as possible on the spine of the scapula (as described earlier), the rhomboid minor is attached on the spine of the scapula just medial to the levator scapulae, and the rhomboid major is attached on the spine of the scapula just medial to the rhomboid minor. Because of the wider insertion of the rhomboid major, its attachment on the medial spine of the scapula is better performed by breaking the bony attachment in its middle part then closing the two edges of the bone (like closing a fish’s mouth) around the medial spine of the scapula ( Fig. 58.5 ).
Postoperatively, patients are placed in a shoulder abduction brace that holds the arm at approximately 70 degrees of abduction for 6 to 8 weeks, depending on the preference of the treating surgeon. Because of the small size of the levator scapulae and rhomboidei, we prefer 8 weeks of immobilization to allow full healing of the transfers and to reduce the risk of stretch injuries from early mobilization. At 8 weeks, patients are started on progressive range of motion for 6 weeks followed by gentle strengthening and aquatherapy for 8 weeks. They are allowed unrestricted activities at 6 months.
Good outcomes have been reported with both techniques, but the EW procedure has been reported to have a better outcome and less risk of failure. , If an EL procedure fails, the only possible remaining muscle transfer option available is to transfer the lower contralateral trapezius origin to the lateral spine of the scapula to restore scapula retraction. The senior author has performed this procedure on five patients with a failed prior EL procedure, and the results were promising in all five cases. The main salvage procedure to stabilize the scapula in symptomatic patients with failed EL procedure is the scapulothoracic fusion. Different techniques have been used to perform scapulothoracic fusion, but most involve passing wires through the scapula and around several ribs with a broad iliac crest bone graft or metallic plate for support. The majority of patients undergoing scapulothoracic fusion achieve good results. However, the complication rate is high, with nonunion rates ranging from 2% to 14%. , Other complications include pneumothorax, pleural effusions, and fracture.
Long thoracic nerve
Anatomy
The long thoracic nerve has a relatively long course after taking origin from the C5, C6, and C7 roots. After crossing over the first rib, it travels 10 to 20 cm to its motor endplates in the serratus anterior. It is vulnerable to blunt trauma over the first rib along the lateral chest wall and can be crushed by forceful displacement of the scapula.
The serratus anterior originates from the upper nine ribs and inserts on the anteromedial border of the scapula. This insertion is only a few millimeters wide at the midportion of the scapula, but it becomes more substantial at the inferior pole of the scapula ( Fig. 58.6 ). It is the inferior portion of the muscle that is important in maintaining protraction and upward rotation of the scapula during forward elevation of the shoulder.
Velpeau first described injury to the long thoracic nerve causing paralysis of the serratus anterior in 1837. Injury to the long thoracic nerve is usually manifested as winging of the scapula. Patients may complain of pain and weakness and have limited forward flexion of the glenohumeral joint. However, winging of the scapula has many possible causes, with multidirectional instability probably being the most common cause of mild winging. Spinal accessory nerve injury can also cause winging, but this injury tends to be milder and results in more of a rotational deformity of the scapula. Some patients have volitional control over the scapula and can demonstrate significant winging at will.
Etiology
The long thoracic nerve is rarely injured as a result of penetrating trauma, but injury can occur during thoracic outlet surgery in the region of the first rib, breast surgery, or lateral chest wall procedures, such as axillary node dissection. , Spontaneous cases of entrapment at the scalenus medius have been described. The most common cause of serratus anterior dysfunction is probably Parsonage-Turner syndrome; indeed, this condition is most likely the underlying cause of long thoracic nerve dysfunction attributed to overexertion, including athletic activities.
Nonoperative treatment
In our opinion, observation should be the standard therapy in idiopathic or nonpenetrating trauma cases. Other than continued use of the shoulder as tolerated, no specific physical therapy protocol has been found to be especially helpful. Braces have been advocated to help hold the scapula against the chest wall. Although these can be somewhat effective, they are usually found to be awkward and are not well tolerated by patients. Most patients with a nontraumatic or idiopathic cause tend to recover from the paralysis and regain serratus anterior function within 6 months to 1 year. Nonoperative treatment may be the preferred option in older and/or low-demand patients.
Operative treatment
At least one-fourth of patients will have symptoms even after 2 years of observation. It is difficult to predict which patient factors will lead to continued pain or dysfunction, prompting surgical intervention. Etiology of the underlying lesion may be an important factor. Electrodiagnostic studies are useful in following the clinical course but have limited prognostic value. Surgical options for treating injury to the long thoracic nerve in the early stages include neurolysis and nerve transfers. Some surgeons have had success with neurolysis of the nerve with decompression at the level of the scalenus medius. However, because it is difficult to ascertain where the lesion resides or if compression (rather than inflammation, for example) is responsible for the dysfunction, we do not recommend this approach for most patients. In cases where there has been no spontaneous recovery by 6 months, another strategy is to perform nerve transfers using one or two intercostal nerves or the thoracodorsal nerve (M.B. Wood, personal communication, 2002.) Nerve transfers obviate the need for precise localization of the lesion because the donor nerve can be transferred close to the motor endplate. This technique has been helpful in several series. Noland and colleagues proposed a treatment algorithm for patients using intraoperative nerve stimulation and preoperative electrodiagnostic studies in patients without signs of recovery by 6 months following injury. Initially, the long thoracic nerve is decompressed in the neck at the level of the middle scalene. Intraoperative nerve stimulation is used to decide whether or not to proceed further with decompression in the chest. This may be followed either by nerve transfer or supercharge end-to-side transfer using the thoracodorsal nerve as a donor, depending on the nerve stimulation findings.
If a patient does not recover serratus anterior function by 1 year and use of the shoulder is compromised, reconstructive options include tendon transfers and scapulothoracic fusion ( Fig. 58.7 ). Scapulothoracic fusion fixes the scapula to the underlying ribs through a variety of techniques. Although this technique will eliminate winging of the scapula, it will decrease shoulder girdle motion by at least 30%, with forward elevation and extension mostly affected. , Complications include pneumothorax, pleural effusions, nonunion, and fracture. For these reasons, scapulothoracic fusion should be reserved as a salvage procedure or for patients with symptomatic facioscapulohumeral dystrophy.
Tendon transfers provide dynamic control of a winging scapula and are our preferred method in patients with a neurologic deficit that has lasted for a year or more. Tubby described transfer of the pectoralis major to the serratus anterior in 1904. Although this transfer might offer initial relief of the winging, the paralyzed serratus anterior tends to stretch out with time and this procedure is not recommended nowadays. Other techniques described include transfer of the pectoralis minor, rhomboids, or levator scapulae.
Transfer of the pectoralis major to the scapula with tendon graft augmentation seems to give the most consistent results. Durman, Ober, and Marmor each described successful transfer of the pectoralis major with a fascial extension graft in a few cases. More recent studies have demonstrated the excellent ability of this tendon transfer procedure to control winging of the scapula. The pectoralis major is ideally suited as a transfer to substitute for the paralyzed serratus anterior. The direction of pull of the pectoralis major is similar to the path of the serratus anterior, and the bulk of the pectoralis major provides enough strength to resist winging of the scapula. The technique has been used with transfer of the entire pectoralis major or with only the sternal head ( Fig. 58.8 ); equally good results have been reported with both procedures. However, the sternal head of the pectoralis major is much more in line with the direction of pull of the serratus anterior than is the clavicular head, and it also provides for a less bulky transfer. Potential concerns of cosmesis or visible deformity of the anterior chest wall should be minimal. In most instances, regardless of whether the entire pectoralis major or only the sternal head is transferred, there is little change in the normal contour of the anterior chest.
This procedure can be performed with a single large incision across the axilla or through two separate incisions. The two-incision technique is not technically harder than a single incision, is somewhat more cosmetic, and is the preferred procedure. The choice of tissue for augmentation of the transferred pectoralis major tendon depends on the surgeon’s preference. The most common choice has been a large portion of fascial lata rolled into a tube. Other graft options include semitendinosus or gracilis autograft of allograft. Fascia lata can be rolled into a spiral tube and draped around the pectoralis major muscle and tendon to provide very strong proximal fixation.
Elhassan and Wagner reported on the outcome of direct transfer of the sternal head of the pectoralis major with its bony insertion to the scapula for patients with symptomatic scapula winging as a result of chronic long thoracic nerve palsy. The senior author has performed more than 200 direct pectoralis transfers, with good to excellent outcome in 86% of patients.
Pectoralis transfer to the scapula augmented with fascia lata is performed with the patient positioned in the lateral decubitus position for easy access to the anterior and posterior aspects of the shoulder and the lateral aspect of the ipsilateral thigh. The anterior approach is usually performed while a second surgical team is simultaneously harvesting the fascia lata. This approach is made somewhat easier by the lateral position. The anterior incision (4 to 6 cm long) is made almost entirely in the axillary crease and is extended only a centimeter superiorly. This technique results in a well-hidden, cosmetic incision. The sternal head of the pectoralis major is easily identified at the inferior margin of the muscle. It wraps posteriorly under the clavicular head and inserts more medial and superior to it. The sternal head is detached directly off the humerus, with care taken to avoid damage to the biceps tendon. The sternal head is then freed up medially onto the chest wall to allow greater excursion of the muscle. The harvested fascia lata graft should measure approximately 14 × 5 cm. The fascia lata is rolled into a spiral tube, draped around the pectoralis major tendon and muscle, and secured with multiple sutures. A heavy running locking suture is then placed through the fascia lata graft and tagged for transfer.
The posterior incision should be made at the junction of the middle and distal lateral edges of the scapula. It is important that an assistant manually pushes the scapula as far anteriorly and laterally as possible. When this position is achieved, a 4-cm incision is made over the lateral edge of the scapula, and the muscles are cleared off the bone and retracted. An 8- to 10-mm hole is created in the scapula with a bur, just medial to the thick lateral mass of the scapula, to ensure a strong bony bridge during the healing period. A large bone hook is helpful at this stage to secure the scapula. Using a large, blunt clamp, a subcutaneous path is created from the anterior incision along the chest wall to the posterior incision. Much of this dissection can be performed with digital palpation. This plane is safe because the brachial plexus is more superior and abducted with the arm.
Once a clear path has been created for the pectoralis major and graft, the traction suture is passed posteriorly and the graft is pulled through the scapular fenestration in an anterior to posterior direction. The graft is then pulled tight, attempting to abut the native pectoralis major tendon to the scapula. The tendon is then folded back and sutured to itself. It is important for the scapula to be held as far anterior on the chest wall as possible while these sutures are secured. No reports of overtight pectoralis major transfers have appeared in the literature. Any excess graft after suture fixation is excised. Drains are not usually needed at closure, and the arm is placed into a sling.
Direct transfer of the bony insertion of the sternal head of the pectoralis major to the scapula is also performed in the lateral position, but the thigh does not need to be included in the surgical field because there is no need for tendon graft. A small anterior incision is performed from the axillary fold proximally for 5 cm; exposure of the pectoralis and the separation of the sternal head from the clavicular head are similar to the technique described earlier. However, when the sternal head is ready to be detached, electrocautery is used to define the bony insertion of the sternal head of the pectoralis major. Before performing the bony detachment, the surgeon can either retract the clavicular head and leave it attached to the humerus or detach it and reinsert it later at the site of the bony defect created at the site of the bony harvesting of the sternal head of the pectoralis major. We prefer the latter because it makes the freeing of the sternal head of the pectoralis major and obtaining full excursion easier. We use a combination of electrical saw and small osteotomes to perform the bony detachment of the insertion of the sternal head of the pectoralis major. Once the tendon is detached with its bony insertion, the tendon is tagged with nonabsorbable suture to facilitate its mobilization and transfer ( Fig. 58.9 ). The remaining steps are very similar to those described earlier, except for the attachment of the tendon. The lower scapula is detached and the lateral distal aspect of it is debrided to obtain bleeding bone ( Fig. 58.10 ). The detached tendon is passed from the anterior to posterior using a grasping instrument ( Fig. 58.11 ), and then multiple (at least five) No. 2 nonabsorbable sutures are placed in a transosseous fashion to be used for the repair. Then, bone-on-bone repair is performed using the sutures as cerclage sutures. If the clavicular head was detached, it is reattached at this time to the proximal humerus at the level of the bone defect that is created from bone harvesting. The technique of attachment is very similar to that for biceps repair.
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