CHAPTER 24 Outcomes of treatment for adult brachial plexus injuries

Olawale A.R. Sulaiman, MD, PhD, FRCS(C), David G. Kline, MD

Summary box

1 Clean, sharp lacerations of the brachial plexus should be repaired within 72 hours. Blunt transections are best repaired in a delayed fashion.

2 Progressive neurologic deficits may be indicative of an enlarging hematoma, arteriovenous fistula, or pseudoaneurysm.

3 Blunt or traction injuries of the brachial plexus that show no evidence of spontaneous recovery have favorable outcomes after surgical intervention.

4 Use of intraoperative nerve action potential recordings is critical for assessing extent of nerve injury and serves to guide the surgeon’s decision-making.

5 Functional outcomes from spontaneous recovery or operative intervention are significantly improved by the use of physical and occupational therapies and secondary reconstructive procedures.

6 Of brachial plexus traction injuries, C5 and C6 injuries have the most favorable outcomes with regard to spontaneous recovery (30%), followed by C5, C6, C7 injuries (16%), and C5–T1 injuries (4%).

7 With brachial plexus traction injuries that progress to surgical intervention, C5 and C6 injuries have the best functional outcomes.

8 C5–T1 lesions remain difficult to repair surgically, and operations are considered salvage-like in nature.

9 Functional outcomes after brachial plexus injuries are improving with advancements in nerve transfer techniques.

10 A limited time window exists for optimal nerve regenerative support and subsequent functional recovery.

Introduction

Management of brachial plexus (BP) injuries has changed significantly over the past century, especially with regard to our understanding of neurobiology, pathophysiology, and pathology of nerve injuries and regeneration, as well as the microsurgical repair of injured nerves.^1,^2,^3,^4,^5,⁶ Advancements in the clinical diagnosis of nerve lesions, development of comprehensive and evidence-based treatment algorithms, and optimization of the intraoperative decision-making process resulting from the introduction of intraoperative nerve action potential (NAP) recordings paved the way for better management of patients inflicted with peripheral nerve and BP injuries.^2,⁷ Another benefit of a rather standardized treatment approach is the ability to systematically study clinical outcomes of patients with nerve injuries after microsurgical repair. Multiple series of functional outcomes after nerve injuries have been reported, both in civilian populations and in war veterans.^8,^9,¹⁰ In this chapter, we discuss briefly our approaches in the management of patients with BP injuries, with particular emphasis on clinical outcomes after microsurgical repair.

Causes of surgical nerve injuries

The BP can be injured either directly as in stab injuries where elements of the BP are sharply transected, or indirectly as in stretch injuries. Recently, traumatic nerve injuries have been classified based on the biomechanics of the injuring processes (Figure 24.1 (part 1)).¹¹ This classification is different from the neuropathologic classification of nerve injuries by Sunderland (Table 24.1), as it emphasizes the mechanism of injury, which is important in deciding the best treatment option for a given nerve injury. BP injuries most often are caused by high energy forces that result in injuries such as transection, contusion, stretch, traction, and/or avulsion. However, BP injuries may also result from compressive neuropathies such as thoracic outlet syndrome, which are due to chronic or repetitive low energy forces (Figure 24.1 (part 2)). BP injuries from injections, radiation, and thermal energy involve rather heterogenous combinations of different injuring factors, but for the purposes of analysis, they are grouped together as a complex group of nerve injuries (Figure 24.1 (part 3)).¹¹

Figure 24.1 Classification of surgical traumatic nerve disorders.

Table 24.1 Nerve injury grading (Sunderland Grading Scale)

Approach to clinical diagnosis

As with every other surgical discipline, the importance of detailed but relevant clinical patient history and mastery of physical examination of the patient as it relates to lesions of the BP cannot be overemphasized. Mastery of these skills combined with prudent use of ancillary tests, such as electromyography (EMG) and imaging studies, will guide the treating physician to an accurate diagnosis and localization of BP injuries (Table 24.2). It is of utmost importance to entertain a broad differential diagnosis and perhaps only accept the diagnosis of BP injury once other causes of upper extremity dysfunction have been considered. This approach is especially important when dealing with controversial diagnostic entities such as Parsonage-Turner and thoracic outlet syndrome. Once a diagnosis of BP injury has been established, surgical treatment of the lesion is dictated by nature of the injury (open versus closed), acuity of the injury (early versus delayed presentation), and findings on clinical, electrodiagnostic, and imaging studies (Figure 24.2).

Table 24.2 Role of nerve conduction studies and imaging in the diagnosis of nerve lesions

With regard to EMG, the following should be emphasized:

EMG should be more than just conduction studies and must include muscle sampling.

Patients can have clinical muscle function despite de-innervational changes.

Patients can have persistent paralysis despite nascents or reduction in denervational changes, such as fibrillation and denervation potentials.

Conduction studies are not always useful, especially for ulnar nerve and brachial plexus cases.

Imaging studies are important, but:

MRI is most useful for tumors; occasionally it may also be useful for entrapments and injury.

To date, in most institutions, MRI is not yet a substitute for CT-myelogram, especially when investigating root avulsions.

Don’t forget plain x-rays! It is possible to pick up parrot’s beak of the C7 spinous process or humeral condyle on plain x-rays.

Figure 24.2 Modified algorithm for surgical management of a brachial plexus injury.

Indications and relative contraindications for surgery

Lacerations of the BP

Transection of the BP may occur when soft tissues surrounding the BP sustain lacerating injuries. These injuries tend to be either sharp or blunt. Sharp injuries to the BP are often caused by stab injuries inflicted by knives, falls through glass windows, or by exploding glass in factory or automobile accidents. Blunt injuries are caused by automobile metal fragments, fan or motor blades, chain saws, and animal bites around the neck.

Patients with lacerating injuries to the BP often have associated vascular injuries and/or airway difficulties; therefore, all initial efforts should be directed toward stabilizing the patient’s potential life-threatening orthopedic or vascular injuries. Securing the patient’s airway, breathing, and hemodynamic stability take precedence over any nerve injuries. Once initial resuscitative efforts are completed, the fundamental goal of managing lacerating injuries of the BP is to establish an accurate diagnosis as soon as possible in an attempt to improve prognosis.

Once diagnosis of a laceration of the BP has been established, urgency of treatment is dictated by the nature of the open wound and the cleanliness of the transected nerve edges:

(a) Sharp nerve transection in a stable, clean soft tissue environment requires primary end-to-end neurorrhaphy within 72 hours.

(b) Progressive neurologic deficit with/without progressive pain syndrome may be indicative of an enlarging hematoma, arteriovenous fistula, or pseudoaneurysm and indicates early intervention with participation by a vascular surgeon.

(c) Nerve laceration within a severely contaminated wound requires aggressive and repeated irrigation and debridement of the wound to remove all necrotic tissues and eliminate risk of sepsis. Delayed repair of the nerve injury is employed, and the method of repair varies from neurolysis, direct end-to-end repair, graft repair and/or nerve transfers, depending on intraoperative findings and NAPs.

(d) Blunt injury to nerve endings at the injury site requires secondary repair. If possible one can “tack down” nerve stumps with a suture to adjacent fascial or muscle planes so that retraction of the nerves is lessened and secondary repair can be achieved by epineurial suture repair instead of graft repair.

Gunshot wound to BP

Gunshot injuries to the BP constitute the second largest category of injuries involving the BP after stretch/contusion. Gunshot wounds to the BP hardly ever require immediate nerve repair because they most often cause neurmas-in-continuity, although in 10% to 15% of cases, blunt transection of BP elements occurs.

Indications for elective nerve repair of gunshot injuries to the BP are listed below:

(a) Complete loss of function persistent in the distribution of one or more elements.

(b) No improvement detected clinically or by electrodiagnostic studies in the early months following injury.

(c) Loss of function in the distribution of at least one element usually helped by operation, such as C5, C6, C7, the upper or middle trunk, or the lateral or posterior cords or their outflows.

(d) Surgery is not performed on injuries restricted to the lower trunks unless pain is a severe problem.

(e) Incomplete loss of function complicated with pain not alleviated pharmacologically.

(f) Pseudoaneurysm, clot, or fistula involving the plexus.

(g) True causalgia requiring sympathectomy.

Stretch Injuries to the BP

Stretch injuries constitute the most common type of injury to the BP and are usually caused by motor vehicle accidents, particularly those involving motorcycles. Stretch injuries to the BP can occur during sports and/or recreational activities such as football, bicycling, skiing, wrestling, gymnastics, and even golf. Regardless of the cause of injury, the biomechanics of stretch injuries always involve distractive forces in which the head and neck are usually pushed in one direction and shoulder and arm in another direction. This results in severe stretch to soft tissues, including nerve and, less frequently, vessels.

Management of stretch injuries to the BP has evolved significantly over the last century, beginning with predominantly non-surgical and musculoskeletal reconstructive operations and amputations to direct surgical repairs. Over the last 2 decades, our understanding of the pathophysiology of poor regeneration and functional recovery has improved significantly and, with it, the evolution of innovative approaches to microsurgical management of BP injuries.^1,^3,^12,¹³ Likewise, better understanding of the natural history of BP injuries with regard to the potential for spontaneous recovery and timing of microsurgical repair has improved our capability to optimize patient benefit from surgical treatment. A combination of suboptimal clinical results despite excellent direct microsurgical repair, and our appreciation of proximo-distal discrepancy in the reinnervation of denervated muscles after BP injuries, created a receptive audience for Narakas when he re-popularized neurotization (ie, nerve transfers) procedures about 3 decades ago.¹⁴ We have adopted an approach to perform direct microsurgical repair for BP injuries whenever feasible, supplemented with neurotization procedures. Our indications for surgical exploration and repair of BP stretch injuries are as follows:

(a) Lack of clinical or electrodiagnostic evidence of spontaneous recovery 3 to 4 months after injury.

(b) Possibility of a direct repair of at least a portion of the BP elements favorable for repair, usually C5, C6, C7 and their more distal outflows.

Approach to intraoperative management of BP lesions

Microsurgery

The key principles in nerve surgery include (1) thorough understanding of the topographic anatomy of the injured nerve (Figures 24.3, 24.4, 24.5); (2) mastery of the required incision and surgical approaches (Figures 24.6, 24.7); (3) adequate surgical exposure of the proximal and distal stumps of the injured nerves as well as the associated nerve branches and blood vessels (Figures 24.8, 24.9); (4) adequate magnification with the use of either the operating microscope or surgical loupes; (5) use of micro-instruments to minimize surgical trauma to the already traumatized nerves and/or branches; (6) careful application of bipolar coagulation only to the epineurial and intrafascicular bleeding points to minimize damage to the nerve itself.

Figure 24.3 The clavicular head of the sternocleidomastoid muscle on the right has been divided to illustrate the location of the phrenic nerve over the scalenus anticus. Once the phrenic nerve has been dissected free and guarded, the scalenus anticus can be divided or a section of it removed after the surgeon has seen that the subclavian artery is free from its posterior surface and the vein from its anterior surface.

Figure 24.4 Sagittal section of left neck at midclavicular level. The spinal nerves that make up the brachial plexus reside in the posterior triangle of the neck by running posterior to the scalenus anticus and anterior to the scalenus medius. The phrenic nerve is bound to the anterior aspect of the scalenus anticus.

Figure 24.5 The infraclavicular brachial plexus resides underneath the pectoralis minor, which need to be mobilized and divided in order to expose the plexus elements.

Figure 24.6 Positioning and incision for anterior exposure of supraclavicular and infraclavicular plexus. Neck incision is just lateral to sternocleidomastoid muscle, angling over clavicle to reach the shoulder. In the shoulder region, the incision runs in the deltopectoral groove.

Figure 24.7 Incision for exposure of the infraclavicular brachial plexus. Incision begins below the clavicle, is in the deltopectoral groove, and runs toward the axillary level.

Figure 24.8 Dissection of supraclavicular plexus on the right side, depicting exposure of spinal nerves, trunks, and divisions of the plexus. The take-off of the phrenic nerve from C4 and the descending plexus are seen, as well as contributions from C5, C6, C7, C8, and T1 to form the upper (C5 + C6), middle (C7), and lower (C8 + T1) trunks of the brachial plexus.

Figure 24.9 Exposure of the entire right infraclavicular plexus. Dissection at this site is difficult as well as tedious. This is especially so when there is scar from prior surgery or extensive injury involving major vessels. Cords of the plexus are positioned around the axillary artery. Note 1) position of the profundus arterial branch between the radial and axillary nerves, 2) medial pectoral branches arising from the medial cord and their interplay with the lateral cord pectoral branches, and 3) origin of the coracobrachialis branch and musculocutaneous nerve from the lateral cord just before the median is formed.

Intraoperative nerve action potential (iNAP)

Lack of clinical and electrodiagnostic evidence of functional recovery 3 to 4 months after nerve injury are indications of lack of adequate reinnervation of denervated muscles and/or remyelination to generate muscle contractions. The senior author (DGK) pioneered the application of iNAP to the evaluation of axonal regeneration across a segment of damaged nerves.^2,⁷ Intraoperative evaluation of axonal regeneration using iNAP is important, because it prevents inadvertent resection of nerves that still have the potential for spontaneous recovery. Appropriate intraoperative surgical decisions can be made with regard to the need for surgical resection of severely damaged nerves that have no response on iNAP (flat) and the subsequent need for direct or graft repair, or neurolysis, and continuation of observant non-surgical treatment if the damaged nerves have positive NAPs. Intraoperative NAPs can also help determine the proximal extent of healthy axons in injured nerves.

In addition, iNAP allows for early evaluation of nerve injuries and a determination of the extent of nerve damage. It can be applied 2 to 3 months after most focal injuries, and 3 to 4 months in less-focal lesions caused by stretch/contusion or gunshot injuries. With its application, the surgeon can sort out the management strategy for approximately 70% of nerve injuries in which nerve segments appear continuous with a variable amount of swelling and/or epineurial scar and yet are nonfunctional. NAP recordings can document the extent of a partial injury or prove that there is a neurapraxic block in the early weeks after the injury. When iNAP is applied months after injury, it can differentiate an axonotmetic lesion (positive NAP across the lesion) from a neurotmetic injury (negative NAP across the lesion).^2,⁷

Nerve repair techniques and nerve grafts

The surgical objective of the repair of any severed peripheral nerve involves either microsurgical realignment of the injured nerve stumps (ie, primary neurorrhaphy) or the use of an autologous nerve graft to bridge a larger defect. A thorough understanding of the surgical anatomy of BP exposure at supraclavicular, clavicular, and infraclavicular levels allows the surgeon to expose key elements of the BP, even after stretch injuries where there is abundant scar tissue formation (Figures 24.10, 24.11, 24.12, 24.13, 24.14, 24.15). Wide exposure of BP elements and the application of iNAP guide the surgeon’s decision-making process with regard to microsurgical repair of injured nerves with or without nerve grafting. The nerve grafting technique was first reported between the years 1870 and 1900, but Hanno Millesi³ re-popularized the concept of using nerve grafts to bridge large defects to avoid the detrimental effects of suturing nerve stumps under tension.¹⁵ His work demonstrated that nerve grafting without tension was superior to epineurial suture under tension, and that tension at the repair site induces scar formation. Therefore, nerve repair without tension is most desirable, because the more scar tissue present at the repair site, the less satisfactory is functional recovery. Tension across a direct suture repair decreases blood flow and promotes proliferation of connective tissue within the nerve, which may block effective axonal regeneration.^6,¹⁵ Acute, excessive stretch may cause intraneural hemorrhage resulting in scar formation and axoplasmic degeneration; subsequent maturation of scar tissue may shrink and constrict nerve fibers and may result in formation of a neuroma-in-continuity.⁶ However, whenever there are small-to-moderate gaps, it may be preferable to mobilize nerve ends to allow direct nerve repair (without tension), which results in better functional recovery than graft repair.