Surgical treatment of brachial plexus injuries

INTRODUCTION — Brachial plexus injuries can cause functional and social disability related to loss of upper limb strength and hand function. When severe injury has occurred, surgical repair may offer the greatest chance of partial recovery.

Surgical management of brachial plexus injuries requires a multidisciplinary approach including physical medicine and rehabilitation, physical and occupational therapists, neurologists/neurophysiologists, and a reconstructive surgeon with expertise in peripheral nerve surgery [1].

The approach to the surgical treatment of brachial plexus injury, including preoperative evaluation, approach to repair, and techniques, is reviewed here. The clinical manifestations and nonsurgical management are reviewed separately. (See "Brachial plexus syndromes" and "Traumatic peripheral neuropathies".)

BRACHIAL PLEXUS INJURY

Anatomy and physiology of injury — The brachial plexus is a network of nerve fusions and divisions that link the brain and spinal cord to the named nerves in the upper extremity (figure 1). Brachial plexus anatomy is reviewed in detail separately. (See "Brachial plexus syndromes", section on 'Anatomy'.)

Nerve dysfunction results primarily from the direct mechanical forces applied to it and any subsequent ischemic nerve damage. Whether the nerve can recover depends upon the severity of injury. Nerve injuries are classified based upon the severity and extent of injury (table 1) [2-4]. Traumatic injuries will cause a combination of neurapraxia, axonotmesis, and neurotmesis in various degrees. Mechanisms of recovery may include resolution of conduction block (in neurapraxic lesions), distal axonal sprouting (in axonotmetic lesions), and axonal regeneration (in axonotmetic and neurotmetic lesions). (See "Traumatic peripheral neuropathies".)

Cervical root lesions and compressions can coexist with distal nerve entrapments along any element of the brachial plexus and terminal named nerves. The double crush syndrome hypothesis proposes that a proximal lesion along an axon predisposes it to injury at a more distal or proximal site along its course through impaired axoplasmic flow and more proximal swelling. Although rare, incidental coexisting distal nerve entrapments have been reported in up to 3.4 percent of electrodiagnostic studies [5]. These may be very difficult to diagnose and may not be apparent until long after the injury when proximal impairment occurred.

Etiologies of brachial plexus injury — Traumatic injuries are the most common cause of brachial plexus lesions in children and adults [6,7]. Mechanisms include transection (eg, penetrating injury), stretch (eg, motor vehicle accidents, sports injuries, obstetric injury), or compression (eg, prolonged pressure during deep sleep or anesthesia, crush injury) [7-9].

Traumatic injury — Traumatic injuries by blunt or penetrating mechanisms can lead to brachial plexus injury due to traction/stretch, contusion/compression, laceration, or a combination of these [10-12]. Traumatic injuries are frequently associated with trauma to the subclavian or axillary artery, with the potential for secondary injury (eg, expanding hematomas, pseudoaneurysm, or arteriovenous fistula). Blunt injuries and blast injuries, including gunshot wounds, can result in variable grades of nerve injuries (Sunderland classification (table 1)) from neurapraxia to complete transection and root avulsion. Penetrating injures such as stab wounds can lead to complete transection of one or more plexus elements. Penetrating injuries warrant early intervention [13]. Scarring from muscle tears and hematomas in the vicinity of brachial plexus elements both in the neck and shoulder can also extrinsically compress the nerves, leading to symptoms of pain and sensory/motor deficits. (See "Severe lower extremity injury in the adult patient" and "Brachial plexus syndromes", section on 'Traumatic plexopathies' and "Traumatic peripheral neuropathies", section on 'Trauma mechanisms'.)

Stretch injuries from trauma, sports, or other mechanisms can lead to both extrinsic and intrinsic nerve injuries. Typically, downward force on the neck and shoulder and movement of the neck in the contralateral direction causes stretch injury to the plexus. These stretch injuries can lead to intrinsic neurotomy, neuroma-in-continuity, or root avulsion. (See "Burners (stingers): Acute brachial plexus injury in the athlete".)

Iatrogenic plexopathy such as postoperative paresis, post-median sternotomy plexopathy, anesthetic block plexopathy, medial brachial fascial compartment syndrome, positioning stretch injures, and pressure injuries can all lead to brachial plexus injury and are described elsewhere. (See "Patient positioning for surgery and anesthesia in adults", section on 'Nerve injury' and "Brachial plexus syndromes", section on 'Nontraumatic plexopathies'.)

Obstetric brachial plexopathy in newborns is attributed to iatrogenic lateral or axial stress to the fetal head and is mainly associated with shoulder dystocia. Upper brachial plexus palsy (C5 and C6) is most commonly followed by addition of C7, and, rarely, the entire plexus can also be involved. The diagnosis is mainly clinical, and management usually involves observation and therapy. Surgical management is needed for select cases if spontaneous recovery does not ensue in three to six months. (See "Neonatal brachial plexus palsy".)

Radiation-induced injury — Radiation-induced brachial plexopathy (RIBP) is a rare adverse side effect due to therapy for malignancy that often does not appear until several years after radiotherapy [14]. RIBP has been reported for head and neck cancers, lung cancer, and breast cancer [15-20]. The pathophysiological mechanisms of RIBP are not completely understood. Radiation-induced neuropathy is attributed to a series of events beginning with direct microvascular injury, ultimately leading to nerve compression by extensive radiation-induced fibrosis causing tightening of the nerve sheath and secondary compression [14,21]. If electromyography shows compression from scarring such as after radiation, these patients can be evaluated and treated in a similar manner to a post-traumatic compression neuropathy. Complete microsurgical neurolysis of the brachial plexus can effectively release extensive radiation fibrosis. Vascularized flap coverage may improve blood supply to the irradiated brachial plexus, improve symptoms, restore function, and decrease the risk of recurrent fibrosis. Longer-standing injuries with complete paralysis may require nerve grafting, tendon transfers, or muscle transfers [21]. (See "Brachial plexus syndromes", section on 'Neoplastic and radiation-induced brachial plexopathy' and "Overview of cancer pain syndromes", section on 'Plexopathies'.)

OVERALL APPROACH — The initial approach to brachial plexus injuries depends on the mechanism and location of the injury, and whether the injury is "open" or "closed." Treatment guided by electrodiagnostic and radiographic studies is individualized to achieve optimal recovery (algorithm 1) [22]. (See 'Timing of surgery' below.)

●Early surgical intervention is warranted for penetrating (stab, gunshot, iatrogenic) brachial plexus injuries (ie, open injuries) that transect the nerve(s). Patients who present with signs of a brachial plexus injury caused by a penetrating mechanism should be referred immediately to a specialist in peripheral nerve surgery. Early surgical exploration and intervention is warranted for sharp or penetrating brachial plexus injuries. (See "Traumatic peripheral neuropathies", section on 'Suspected nerve transection' and 'Timing of surgery' below.)

●For blunt or stretch mechanisms (ie, closed injuries), patients should be referred to a specialist in peripheral nerve surgery for evaluation in a timely (one to two weeks) fashion. Treatment is initially conservative with follow-up evaluation that includes serial examinations, electromyography (EMG), and imaging for symptoms that do not improve. EMG may be repeated before considering intervention. The natural history of traumatic brachial plexopathies is not well documented, but most natural improvements occur within six months. This does not justify a "hands-off" approach until the six-month mark, but rather active surveillance with operative intervention at an appropriate juncture. (See "Traumatic peripheral neuropathies", section on 'Nerve not likely transected'.)

PREOPERATIVE EVALUATION — Preoperative evaluation of the patient involves a detailed history, meticulous examination, and radiographic and electrodiagnostic studies. Traumatic injuries may include a combination of plexopathy and root avulsions [7,23]. It is critical to differentiate between intraplexus injuries (postganglionic) and root avulsion injuries (preganglionic) since the surgical treatment can be completely different (algorithm 1). Root avulsion injuries may require distal transfers from uninjured nerve roots. Clinical examination, radiographic evaluation, and electrodiagnostic studies aid in distinguishing these anatomical sites. (See 'Imaging' below and 'Electrodiagnostic testing' below and "Brachial plexus syndromes", section on 'Root avulsions'.)

History and physical exam — Surgical planning includes an examination that identifies and confirms neurologic deficits. A detailed history including mechanism of injury, timing of onset, improvement or worsening, sensory and motor symptoms, as well as assessment of pain and quality of life is important in guiding appropriate diagnostic studies and the surgical plan. The authors take videos of all patients to document the initial exam and progress during surgical treatment.

Next, the surgeon must identify which "spare parts" (ie, functioning muscles or nerve donors) are available for reconstruction. Individual muscles should be separated from groups of muscles during the examination. If clinically not feasible, then selective or superselective electromyography may be helpful. Similarly, flaccid paralysis has to be differentiated from spastic paralysis as both can result in lack of function in the upper extremity, but treatment may be completely different. Spastic paralysis is much more complicated in terms of diagnosis, differentiation, and treatment. Spastic paralysis needs to either be substantially weakened or converted to flaccid paralysis prior to attempts of reinnervation. Finally, the surgical assessment includes the possibility of a backup plan if the initial plan does not give optimal results.

The clinical evaluation for surgical planning can be summarized as follows:

●What functions are missing (eg, elbow flexion)?

●What functions are interfering with others (eg, internal rotation limiting elbow flexion)?

●What functions can be/are desirable to be restored (eg, pronation/supination may be less worthwhile to restore compared with elbow flexion)? What is the hierarchy of function?

●Which donors can be used to restore function (ie, which donors have to be sacrificed)?

●Which new donors can be created to restore function?

●Are there any non-neural limitations to functional restoration (eg, bone/joint injury, contracture, and cognitive issues)?

Assess motor function — The motor deficit may be the most obvious defect but may not necessarily be the most important depending on the location of the injury. (See 'Assess sensation and pain' below.)

First, examine the active and passive range of motion of all joints prior to testing the muscles. Passive range of motion should be inspected first before active range of motion. Individual muscles should be evaluated (eg, different heads of triceps). Manual palpation of muscles should be performed to differentiate between spastic versus flaccid paralysis. Again, when dealing with peripheral nerve injuries, only flaccid paralysis needs to be assessed.

A comparison should be made with the contralateral side. The authors use the British Medical Research Council muscle grading system (M1 to M5) to document muscle function (table 2). Muscles should be tested in a gravity-neutral position; as an example, the biceps are tested with the arm in 90-degree abduction.

Assess sensation and pain — The sensory exam includes a somatosensory exam of the supraclavicular region and entire upper extremity as well as the presence of Horner syndrome (meiosis, enophthalmos, upper eyelid ptosis, and anhydrosis). Horner syndrome is a strong indicator of avulsion of C8 and T1 roots. Tinel's sign should always be assessed and recorded; serial examination postoperatively guides the surgeon regarding regenerating distance over time.

For many patients, especially those with paralysis, the most important functional consideration is unremitting pain. The onset, duration, and frequency of pain and any history of radiation treatment should be documented. Pain severity can be recorded using the visual analog scale. Pain management consultation is very useful. The authors document all pain medication usage pre- and postoperatively to monitor pain medication usage.

Pain in brachial plexus injuries is associated with interruption of afferent nerve signals (deafferentation pain). Pain may be from four possible causes: (1) direct nerve pain, (2) neuroma, (3) joint subluxation and orthopedic derangement, and (4) phantom limb syndrome [24-26].

A patient with brachial plexus injury may not have distal motor targets for optimal functional recovery but may still benefit from excision of neuroma or a nerve graft for pain relief. Similarly, tendon transfer such as a trapezius to deltoid transfer may alleviate the pain from shoulder subluxation [27]. Following surgical treatment for brachial plexus injury, pain scores are often lower compared with before surgery and are postulated to be related to rerouting of disrupted sensory axons regardless of the degree of motor recovery. Reduction in pain can improve participation in therapy and indirectly improves motor recovery [13,28,29].

Assess potential donor nerves — For surgical planning, not all nerves are equal. There are a number of key factors in selecting the donor nerves.

What loss of function will occur after transfer? One strategy to minimize this loss is using a branch of the nerve after arborization of its crucial branches. Another is to use a nerve to a muscle that is either synergistic or no longer functional after the patient's injury. As an example, if a patient is unable to move his/her shoulder, the stabilization of the scapula by the serratus anterior via the long thoracic nerve is no longer an issue. In this situation, the long thoracic nerve becomes an excellent donor [1].

What is the length of the defect? This will determine whether additional nerve graft is required with the nerve transfer (ie, neurotization), which unfortunately will decrease the success rate. As an example, the spinal accessory nerve will reach the suprascapular nerve for neurotization but may require additional graft to reach the axillary nerve [1].

Where is the injury relative to the motor end organ? If the nerve has to travel a long distance after neurotization, the likelihood of a successful result diminishes considerably. A classic example of this is the "babysitting procedure," using a nerve transfer closer to the end organ to preserve motor end plates ("trickle charge") until the intended axon regrowth can reach the target muscle. A more proximal neurotization would be much less likely to reinnervate the small interossei within a reasonable time frame prior to motor end plate degeneration and muscle atrophy [1].

Another key concept in choosing donors is that of axonal density, essentially a relatively high number of axons for the nerve diameter. It is important to choose donor nerves that will allow the patient to obtain meaningful movement, which is more than simply movement against gravity. The surgical result will be optimized when the donor and recipient nerve are matched in terms of total diameter and average axonal density [1,30-33].

Imaging — Plain radiographs aid in the diagnosis and can also help guide surgical planning. As examples:

●An inspiratory and expiratory chest radiograph can determine whether there is phrenic nerve paralysis.

●Rib fractures indicate underlying damage to intercostal nerves and may preclude their use as donor nerves.

●Cervical spine fractures may indicate injury to the corresponding nerve roots.

●Scapular fracture may indicate injury to the suprascapular nerve.

●Humeral fracture may indicate injury to the radial nerve.

Arteriography of the upper extremity can be helpful to determine the status of the vasculature or other vascular issues (eg, pseudoaneurysm), particularly in those with history of previous vascular trauma. Cross-sectional imaging such as computed tomographic (CT) myelography [34] and T2-weighted magnetic resonance (MR) imaging [35] helps determine nerve root integrity and aids in the diagnosis of pseudomeningocele or partial or complete root avulsion.

Electrodiagnostic testing — Electrodiagnostic testing provides information regarding the location, severity, and prognosis of the nerve injury (table 1). (See "Traumatic peripheral neuropathies", section on 'Diagnosis'.)

Nerve conduction studies and needle electromyography are the cornerstone of diagnosis in brachial plexus injuries and are described in detail elsewhere. (See "Overview of upper extremity peripheral nerve syndromes", section on 'Overview of diagnostic testing'.)

These studies are also important for the assessment of donor nerves and surgical planning. Their results are especially meaningful when performed in sequence over a period of time (algorithm 1).

PATIENT PREPARATION

Timing of surgery — Timely surgical intervention in brachial plexus injuries can determine the ultimate functional outcome. Early surgical intervention is warranted for sharp or penetrating brachial plexus injuries [36].

After a blunt or stretch injury, the authors obtain electrodiagnostic studies at six weeks and then at three months. If there is no improvement in three months, surgical planning is initiated (algorithm 1). Regardless of the timing of surgery, these patients require therapy before and after surgery to prevent contractures of the involved joints. A systematic review suggested that surgical intervention at three months optimizes recovery [22].

In addition to mechanisms of nerve recovery (eg, axonal sprouting, axonal regeneration), recovery also depends upon the integrity of the muscle when the nerve reaches it. The structural architecture of the muscle and the end plate integrity can be maintained to a certain degree for up to one year, but after two years complete irreversible muscle fibrosis will have occurred along with muscle degeneration, leading to a permanent loss of functional muscle tissue. Under these circumstances, nerve transfers may not yield meaningful functional recovery [12,37-39]. (See "Traumatic peripheral neuropathies", section on 'Mechanisms of functional recovery'.)

Informed consent — Any nerve reconstruction or transfer involves risks that may include loss of donor nerve function. The process also requires a long waiting time to reinnervation depending on the level of injury and prolonged therapy (figure 2). Despite best efforts, functional recovery may be suboptimal. Hence, it is critical to ensure that the patient fully understands the risks and benefits of surgical intervention. (See "Informed procedural consent" and 'Postoperative care and rehabilitation' below.)

The overall course of reconstruction can span years. Nerve surgery can take over one year to yield results. Rehabilitation from these procedures often takes many months between steps before moving onto other secondary and tertiary procedures. Tendon transfers must be performed stepwise in order not to compete with rehabilitation protocols. The determination of whether additional steps are needed often cannot be made until after nerve surgery recovery. The course of treatment can be long and arduous but also rewarding in terms of function, pain reduction, and decrease in disability. (See 'Postoperative care and rehabilitation' below and 'Tendon transfers' below.)

TECHNIQUES FOR MANAGING TRAUMATIC INJURIES — The main goal of surgery is to restore motor and sensory neurologic function [40,41]. Specific surgical techniques are used based on the type of nerve injury, as described in the next sections.

Surgery is performed typically under general anesthesia, though without the use of paralytic agents, and with intraoperative neuromonitoring to guide surgery.

For blunt trauma and traction injuries, often times both the supra- and infraclavicular plexus are explored and the diagnosis is made or confirmed intraoperatively. Surgical exposure for the brachial plexus involves an incision along the posterior border of the sternocleidomastoid, which is extended posterolaterally. For infraclavicular exposure, it is extended to the deltopectoral groove. Supraclavicular nerves, the external jugular vein, transverse cervical vessels, and the cephalic vein are preserved.

For nerve lesions apparently in continuity, the surgical approach differs based upon the results of direct intraoperative nerve stimulation. If nerve action potentials are present, nerve decompression (ie, neurolysis) is the preferred approach. If no nerve action potentials are recorded, nerve reconstruction or nerve transfer (ie, neurotization) is performed.

Nerve decompression — The surgical approach to nerve decompression (ie, neurolysis) due to entrapment depends on the site of entrapment. There are multiple potential compression sites including scarring resulting from trauma. Other known sites of compression are implicated with traumatic thoracic outlet syndrome such as the scalene muscle, cervical rib, first rib, and clavipectoral fascia [1].

Microneurolysis is performed when explored elements of plexus are hard to palpate. Thickened epineurium compresses the axons and bundles. To relieve the intraneural pressure, longitudinal epineurotomy can be performed under the operating microscope. This can be extended to the perineural or interfascicular level. Bulging of released fascicles is usually an indicator of effective microneurolysis.

Nerve reconstruction — During exploration, the presence of a neuroma is usually an indicator of intact proximal nerve root. With adequate preoperative assessment of nerve root integrity and intraoperative stimulation, the proximal stump can be used as an intraplexus donor nerve. Proximal nerve stump dissection to healthy fascicles provides the highest number of donor axons compared with any other extrinsic nerve transfer provided the nerve root is intact. These neuromas-in-continuity can sometimes pose a significant dilemma if there is some function preserved across the injury site. Nerve stimulation in these cases can guide the decision to perform microneurolysis versus resection with interposition nerve grafting. The sural nerve graft is the most common donor site for nerve graft and can be used for multiple nerve grafts and cable grafts.

Nerve transfers — Nerve transfers remain the mainstay of treatment, especially when proximal roots are avulsed. Nerve transfers include intraplexus and extraplexus nerve transfers from nerves that have not been injured. Distal nerve transfers have gained popularity, with the advantage of providing reinnervation close to the distal targets and a shorter time to reinnervation.

Nerve transfers for elbow flexion — The ulnar to musculocutaneous nerve transfer (ie, Oberlin) involves the transposition of fascicles of the flexor carpi ulnaris to the biceps branch of musculocutaneous nerve [42]. This can be combined with the median nerve branch to brachialis branch of the musculocutaneous nerve (Mackinnon or double transfer) [43]. The average time to reinnervation in these transfers is five months, which is considerably shorter than plexus reconstruction using interposition grafts.

An alternative donor is the thoracodorsal nerve to musculocutaneous nerve without actual latissimus transfer for elbow flexion. The medial pectoral nerve can also be transferred to the musculocutaneous nerve as donor.

Extraplexus donors also exist to reinnervate the musculocutaneous nerve. Spinal accessory to musculocutaneous transfers and intercostal to musculocutaneous transfers can both be effective in restoring elbow and shoulder function. While spinal accessory transfers have a better outcome for return of shoulder function, intercostal transfers have been reported to provide better results for restoration of elbow flexion. In a review of 1088 nerve transfers from 27 studies, direct intercostal transfers to the musculocutaneous nerve had a better ability to achieve ≥M4 elbow strength (table 2) compared with transfers from the spinal accessory nerve (41 versus 29 percent) [44].

Nerve transfers for shoulder and rotator cuff function — The nerve to the long head of triceps (pure motor nerve) can be transferred to the axillary nerve and has shown 100 percent recovery of shoulder abduction and 85 percent recovery of external rotation when surgery is performed in a timely fashion [13]. When the triceps nerves are not available, a medial pectoral to axillary nerve transfer may be considered. The distal trapezius branch of the spinal accessory nerve can also provide a suitable donor for transfers within the neck region. Another standard treatment option in some algorithms is a spinal accessory to suprascapular nerve transfer. The spinal accessory nerve has functional characteristics similar to those of the suprascapular nerve and has been reported to achieve up to 95 percent shoulder abduction recovery following a transfer procedure [13,45]. The spinal accessory nerve may also be used for a musculocutaneous nerve transfer with interposition grafting.

Nerve transfers for lower trunk injury — Fewer options are available when planning a nerve transfer for a lower trunk injury.

Other extraplexus transfers, such as the contralateral C7 nerve root, are available as a donor but are less optimal due to the long distance to regeneration. Similarly, intercostal nerves have significantly fewer numbers of motor axons, and harvest is time consuming. However, in certain cases, these methods can be effective in achieving M3 and M4 results (table 2). The authors prefer the dual approach: reconstructing the plexus as well as distal transfers.

Free functional muscle transfers — Neurotized free gracilis muscle can be used to restore elbow function if the time to reinnervation is delayed to an extent that motor end plates have degenerated. Free gracilis transfers can also be used for finger flexion or extension [46-48]. Free gracilis muscle is harvested with a branch from the obturator nerve and anastomosed to the recipient vessels in the neck, axilla, or arm.

Alternative options include rectus femoris and latissimus dorsi muscle transfer. Ipsilateral extraplexus donors such as spinal accessory or medial pectoral and intercostal nerves can also be used for neurotization.

Tendon transfers — Several tendon transfers have been described for brachial plexus injuries, and the choice depends on the functional deficits and donor availability. Typically, tendon transfers are performed for delayed presentations after the motor end plates have degenerated. Tendon transfers for flexion and those for extension are not performed simultaneously due to competing rehabilitation.

The muscle to be transferred needs to be adequately innervated and should have at least M4 strength (table 2). With functioning trapezius, clavicular and acromion insertions of trapezius can be transferred to the humerus to aid in shoulder abduction. Rerouting the latissimus dorsi muscle for external rotation of the shoulder has also shown promising results in obstetric brachial plexopathy.

Pedicled latissimus and pectoralis major muscles have also been used to restore elbow flexion. A Steindler flexorplasty using flexor-pronator advancement proximally on the humerus can also provide flexion at the elbow. Triceps to biceps transfer has been reported in the literature but did not gain popularity due to problems with elbow joint stabilization.

Joint fusion — The wrist joint can be stabilized through fusion to provide effective hand reanimation from existing finger flexors, or as an adjunct to tendon transfers for hand animation.

Scapulohumeral arthrodesis has been published in the literature but did not gain popularity due to limited functional benefit.

Other orthopedic interventions include rotational osteotomy of the humerus for external rotation with promising results in delayed treatment of Erb's palsy.

Targeted muscle reinnervation — Nerve transfers can also be performed to provide intuitive prosthetic control to upper extremity amputees. Targeted muscle reinnervation (TMR) has provided coordinated control of prostheses through intra- and extraplexus transfers. (See "Upper extremity amputation", section on 'Target muscle reinnervation'.)

It is important to consider future TMR for bioprosthetic devices while planning for surgical treatment of brachial plexopathy. These devices continue to improve at a rapid pace and hold great potential for future functional improvements for patients with severe injuries. These devices rely on signals acquired from muscles just above the amputation sites. As an example, in transhumeral amputation (figure 3), the terminal end of the median nerve is coapted to the motor branch to short head of the biceps and the terminal radial nerve to the motor branch to the triceps. Signals acquired from contraction of these muscles then guide the prosthesis to close and open its fingers. For higher levels of amputation (figure 4), motor branches to the pectoralis major, latissimus, and serratus can be used as targets for musculocutaneous, radial, and medial nerves as they exit the plexus. The aforementioned muscles can then be used as proxy signals for the respective functions of these nerves [49,50]. One must be cognizant that the nerves to power this TMR may be rendered nonfunctional in brachial plexus injuries, and therefore, extraplexus donors may be more useful.

POSTOPERATIVE CARE AND REHABILITATION — All patients are placed in a custom-fitted brace postoperatively. Typically, for brachial plexus exploration and nerve reconstruction, the upper extremity is kept at 45-degree abduction and a neck collar is placed for protection of any graft repair. The patient usually stays in the brace for three to six weeks. Hand and wrist custom splints are used if involved to keep the wrist extended, metacarpophalangeal joints flexed, and remaining joints in functional position.

Postsurgical rehabilitation starts immediately with range of motion exercises depending on the extent of nerve grafts and reconstruction (figure 2). Effective communication between the surgeon and therapist is key to successful therapy. Therapy is started away from surgical sites, and once the brace is removed, full passive and active range of motion exercises are started. Often times the donor nerve function has to be elicited to get response in recipient muscle groups.

Functional outcomes — Outcomes following brachial plexus surgery depend upon the nature and severity of injury as well as the experience of the surgeon with brachial plexus injuries. Overall, improved function is seen in approximately 60 percent of appropriately selected patients after surgical intervention [51]. However, with careful surgical planning, the rates of functional improvement by specific surgical interventions have been reported to be much higher in select patient cohorts. Rates of successful functional improvement following neurolysis, direct/primary nerve repair, nerve transfer, muscle transfer, or tendon transfers have been reported to be as high as 83 to 96 percent [26,52-54].

Two of the major limitations in peripheral nerve regeneration are the slow pace of regeneration and the long distance of regeneration to end targets. Both these factors significantly impact the degree of functional recovery and often result in a variable degree of end plate degeneration. Several studies are ongoing to look at the role of innovative therapies such as stem cells and growth factors for improving and enhancing nerve regeneration [55,56].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Severe blunt or penetrating extremity trauma".)

SUMMARY AND RECOMMENDATIONS

●The brachial plexus is a network of nerve fusions and divisions that link the brain and spinal cord to the named nerves in the upper extremity. Disruption of the nerves of the brachial plexus can be debilitating both functionally and socially. Injury to the brachial plexus results primarily from mechanical forces (ie, transection, stretch, compression) applied to it and any subsequent ischemic nerve damage. Most traumatic nerve injuries involve a combination of mechanisms. (See 'Anatomy and physiology of injury' above and "Traumatic peripheral neuropathies".)

●Surgical evaluation for brachial plexus injuries involves a thorough history and physical examination, imaging, assessment of motor and sensory deficits and pain, electrodiagnostic studies, and identification of potential donor nerves. (See 'Overall approach' above and 'Preoperative evaluation' above.)

●Brachial plexus injuries need to be treated in a timely fashion before muscle damage is irreversible. A combination of nerve reconstruction and nerve transfers from intra- or extraplexus functioning donor nerves can provide both functional benefits and pain relief. For delayed presentations, tendon transfers and joint fusion can provide functional improvements. (See 'Timing of surgery' above and 'Techniques for managing traumatic injuries' above.)

●A multidisciplinary approach including a neurologist, physical medicine and rehabilitation, occupational therapy, and reconstructive surgeons with expertise in peripheral nerve surgery is critical in achieving optimal functional recovery. (See 'Introduction' above and 'Postoperative care and rehabilitation' above.)