Neurological Complications and Shoulder Arthroplasty

Bertrand Coulet, MD, PhD

Geert Alexander Buijze, MD, PhD, FEBHS

Pierre-Henri Flurin, MD

INTRODUCTION

Neurological complications following shoulder arthroplasty are not frequent, with a reported incidence of less than 5%, but are probably underestimated since a majority spontaneously recover.¹ Nevertheless, in unfavorable cases, often affecting elderly patients with reduced neurological regeneration potential, their management is not straightforward. For the purpose of this chapter, we have designed a decision-making algorithm for the treatment of neurological complications after shoulder arthroplasty, based on a review of the neuroanatomy of the shoulder, the pathophysiology of these complications, and their neurological and palliative management.

SHOULDER NEUROANATOMY

The shoulder has two articular systems, scapulothoracic and glenohumeral (GH), each consisting of two muscle groups with their own innervation (FIGURE 39.1). The scapulothoracic system has a posterior group, whose main motor is the trapezius, innervated very proximally by the eleventh paired cranial nerve (accessory nerve), and an anterior one, the most important of which is the serratus anterior innervated by the long thoracic nerve, originating from the C5-C7 nerve roots of the brachial plexus. The GH joint also has two muscle groups. The first includes the rotator cuff muscles, including the supra– and infraspinatus, which are innervated by the suprascapular nerve arising from the superior trunk of the brachial plexus, as well as the teres minor innervated by a branch of the axillary nerve (AN) and the subscapularis innervated by two individual branches. The second muscle group includes the deltoid innervated by the terminal branch of the AN arising from the posterior cord.

This double innervation pattern and the presence of these two systems imply that complete paralysis of the shoulder is exceptional, except in the case of very proximal lesions, and that there is important potential for compensation, within the same system and also between the two systems. This important concept explains the delays in the diagnosis of certain deficits that can be perfectly compensated for.

The proximity of the brachial plexus and its terminal branches is one of the causes of neurological complications during arthroplasty, through direct injuries (blunt or compression) and especially through stretching (FIGURE 39.2).

The suprascapular nerve has a short trajectory after its emergence from the superior trunk and presents several points of vulnerability. The first point is at the suprascapular notch before entering the supraspinatus fossa, where it constitutes a fixed point making it particularly vulnerable to traction. The second is located in the spinoglenoid notch, a crossing point between supra– and infraspinatus fossae. These two zones are in direct contact with the glenoid, where the center of the articular surface is located at 28 and 12 mm, respectively, in the anterosuperior and posterosuperior planes.²

The axillary nerve, upon emergence, has a posterior trajectory less than 11 mm from the lower capsule of the GH joint.³ Its exit from the quadrilateral space as it winds around the humerus constitutes a point of fixation and, above all, a zone of close contact with the humeral metaphysis (5-8 mm).¹,⁴ The AN will therefore be vulnerable during any procedure involving the lower part of the capsule, and also by traction when the internally rotated humerus is translated posteriorly. An anterosuperior approach is not without risk. As Burkhead et al⁵ have shown, the classic mean safety distance for the AN of 50 mm below the acromion is reduced to 30 mm in abduction.

After its emergence, the radial nerve has a more direct path but several points of vulnerability. The first is the passage under the latissimus dorsi tendon and its insertion zone, the proximity of which varies greatly depending on the position of the arm, as shown by Gates et al.⁶ In adduction-internal rotation, this distance is minimal (15 mm), whereas it is maximal in abduction-external rotation (52 mm). The second is the area where the radial nerve wraps around the humerus, constituting a point of fixation, but, above all, an area of close contact with its gutter, making it particularly vulnerable in the event of fracture or cement extravasation.⁷,⁸

FIGURE 39.1 Schematic presentation of the neuroanatomy of the shoulder with the two-joint systems represented. The scapulothoracic system with its two main motors and their proximal innervation, the trapezius innervated by the accessory nerve (eleventh cranial nerve) and the serratus anterior innervated by the long thoracic nerve. The glenohumeral system with the rotator cuff innervated by the suprascapular nerve and the deltoid innervated by the axillary nerve.

More medially, the area where the musculocutaneous nerve crosses the coracobrachialis muscle represents an area of potential direct trauma by a retractor and also of point of fixation subject to stretching injury. The other nerves of the brachial plexus are more distant but can be damaged indirectly by a traction mechanism. As in obstetric lesions, it is the upper roots and trunks that will be most vulnerable because of a vertical traction vector.

CLASSIFICATION OF NERVE INJURIES AND GENERAL CONSIDERATIONS

Pathophysiology and Classification

There are two types of nerve lesions: (1) the frank disruption without any possible spontaneous recovery, and more frequent in the shoulder; (2) continuous lesions as a result of traction or crushing, whose prognosis of spontaneous recovery is very variable depending on the extent of the trauma.

Seddon,⁹ followed by Sunderland¹⁰ (TABLE 39.1), classified these nerve injuries according to the nature of the lesion and prognosis. The importance of the axonal trauma was emphasized, from a simple injury (neurapraxia) recovering spontaneously in a few weeks to a more important injury with distal Wallerian degeneration, the recovery of which is conditioned by the integrity of the nerve sheaths. If the basal lamina of the Schwann cell is intact, the nerve sheath guides the regeneration of axons (axonotmesis) and recovery is possible but takes longer and is often incomplete. This regrowth depends on the patient’s capacity for axonal regeneration (important factors include age and tobacco use) and the type of nerve involved. Conversely, if the nerve sheath for axonal regrowth is destroyed (neurotmesis), although the nerve is in continuity, axonal regeneration is impossible.

Mackinnon described an additional type¹¹ in which these different stages exist in the same nerve for different fascicles and at several levels, constituting mosaic lesions at the origin of an early recovery whose progression stagnates rapidly.

Mechanisms of Injury

Several mechanisms can cause nerve damage in the shoulder with varying consequences:

A nerve section is the most obvious, the deficit is complete without spontaneous recovery.
A stretching mechanism is by far the most common. It will be more severe with greater displacement and occurs along the axis of the nerve over a short
segment. This mechanism can affect several nerves at the same time.
A crushing mechanism by a retractor or a blunt instrument.

FIGURE 39.2 Representation of the areas of vulnerability of the nerves around the shoulder. Red represents the areas of potential direct trauma, and blue represents the points of nerve fixation that could cause traction injuries. AN, axillary nerve; CBM, coracobrachialis muscle; MCN, musculocutaneous nerve; MN, median nerve; RN, radial nerve; SScN, suprascapular nerve; UN, ulnar nerve.

Nagda et al¹² performed intraoperative nerve monitoring during total shoulder arthroplasty (TSA). They showed signs of nerve alertness in 57% of the shoulders, regressive after neutralization or removal of the retractor, but almost half retained postoperative disturbances based on electroneuromyography (ENMG). They observed diffuse involvement of the brachial plexus in 50% of cases and of the musculocutaneous nerve and AN in a comparable manner in 20%. Shinagawa et al,¹³ with a similar monitoring method during reverse TSA (RTSA), showed that the AN is the most vulnerable, especially during the preparation of the humerus and the glenoid. Lenoir et al¹⁴ reported an anatomical study of the tension (stress) on the nerves during the insertion of an RTSA. They observed significant increases in tension on the axillary and radial nerves during exposure of the humerus when it is in a position of internal rotation and extension. External rotation becomes potentially hazardous beyond 45° except for the AN and above 60° for all nerves when associated with extension. Furthermore, exposure of the glenoid increases the tension on the axillary, radial, and musculocutaneous nerves, especially during posterior translation of the head. A polyethylene insert greater than 3 mm also potentially increases tension on the axillary, radial, and musculocutaneous nerves. Inserts larger than 9 mm can impact all the nerve structures.

Epidemiology

Neurological complications after shoulder arthroplasty are underestimated, with an incidence reported to be less than 1% in the overall literature.¹⁵,¹⁶,¹⁷,¹⁸ However, this complication when actively sought, is more common, as Lynch et al¹ observed it in 4.3% of shoulder arthroplasties. The incidence is increased in women without any association to the patient’s morphology and also in cases of revision, rheumatoid arthritis, or osteoarthritis and in those with significant limitation of preoperative
external rotation. The diagnosis is delayed in the majority of cases. Two-thirds can be expected to recover within 6 months. More than half of the cases that do not recover have an AN paralysis. Injury to the radial nerve is mainly related to cement extravasation or fractures of the humerus. More recently, Kim et al¹⁹ and Ball et al¹⁵ showed that RTSAs resulted in a 20% incidence of neurological deficit due, in part, to the distalization of the construct. The AN was affected in almost 50% of cases, followed by the radial nerve in 20%, the musculocutaneous nerve in 10%, and the median nerve in 10%. In these series of RTSAs, the suprascapular nerve was injured by protruding glenoid screws.

TABLE 39.1 Different Types of Neurological Lesions According to the Seddon and Sunderland Classifications Including Their Clinical and ENMG Presentations and Prognosis

		Degree of Nerve Injury		Prognostic	ENMG
Nerve Injury	Histopathologic Changes	Seddon Classification	Sunderland Classification	Recovery	Fibrillations
	Axon: nerve conduction bloc No Wallerian degeneration Muscle: no denervation	Neurapraxia	Type I	Spontaneous, fast (few weeks)	None
	Axon: stop of nerve conduction Wallerian degeneration Intact basal membrane Axonal regeneration Muscle: denervation	Axonotmesis	Type II	Spontaneous, slow, complete	Present
	Axon: stop of nerve conduction Wallerian degeneration Intact basal membrane but injured myelin sheath Axonal regeneration Muscle: denervation		Type III	Spontaneous, slow, incomplete like “perfect nerve repair”	Present
	Axon: stop of nerve conduction Wallerian degeneration Injuries of all nerve sheaths—nerve appearing macroscopically in continuity No axonal regeneration Muscle: denervation	Neurotmesis	Type IV	No recovery	Present
	Complete nerve section		Type V	No recovery	Present
	Mixed injury (Mackinnon)		Type VI	Variable	Present

RTSAs are particularly at risk for several reasons including the more extensive mobilization of the humerus due to the frequent absence of the rotator cuff and the inherent distalization of the humerus.⁴,⁵,⁶,⁷,⁸,⁹,¹⁰,¹¹,¹²,¹³,¹⁴,¹⁵,¹⁶,²⁰ The prognosis for these lesions is generally good with almost 90% being neurapraxias and an average recovery time of 7 months for the AN and 5 to 6 months for the other nerves. Finally, the deltopectoral approach seems to place the nerves at greater risk, especially in the absence of release of the anterior fibers of the deltoid, perhaps as a result of excessive stress on retractors.

TOWARD A SURGICAL STRATEGY

When faced with a neurological complication following TSA, it is possible to adopt a standard approach that is applicable to all lesions (TABLE 39.2).

The first stage (initial phase) consists of establishing the precise identification of the lesion, topography, mechanism, and the impact of the neurological deficit
on the outcome of the arthroplasty. This analysis should make it possible to answer three questions that will determine management:

TABLE 39.2 Management of a Neurological Complication After Shoulder Arthroplasty From the Initial Phase to the Sequelae Stage

Should immediate surgical intervention be considered?
What impact will this paralysis have on the short- and long-term function of the arthroplasty?
What is the prognosis of the lesion in this patient, and is spontaneous recovery possible?

The second stage is a recovery and follow-up phase. Regardless of whether or not revision surgery has been performed, specific clinical and paraclinical evaluation criteria are established, with a time limit beyond which the absence of recovery must prompt reconsideration of the treatment plan.

The third stage occurs 4 to 6 months after the initial operation (or revision surgery if it was necessary) with a
careful evaluation of the initial strategy and the results with the goal of determining a definitive treatment plan:

If the patient is recovering, the plan should continue with an increased emphasis on rehabilitation.
If there are no clinical and paraclinical signs of recovery, management should be redirected based upon axonal regeneration capacity and the functional impact of the paralysis. If the patient has some potential for axonal regrowth, a neurological intervention may be considered; otherwise, the patient will be directed toward the final phase which is neurological consolidation.

The phase of neurological consolidation corresponds to the stabilization of the neurological status when recovery is no longer progressing. At this point recovery may be significant or minimal to none. The recovery and the impact of the residual motor deficit on function are assessed followed by discussion, if necessary, of tendon transfers or joint stabilization procedures.

Initial Evaluation—Diagnostic Circumstances

The immediate postoperative diagnosis is not always obvious, as the neurological examination of the shoulder is often masked by pain or impossible in the case of analgesic peripheral nerve catheters or prolonged regional anesthetic blocks.

Overall, three main circumstances may be encountered:

Concern about a technical (iatrogenic) intraoperative complication or maneuver (aggressive periarticular release, diaphyseal fracture of the humerus): In this situation, a careful assessment of the deficit is needed (excluding local analgesia). Once the diagnosis is established a decision concerning immediate operative intervention is made.
Complete or partial (distal) upper limb deficit involving the hand or elbow in the immediate postoperative phase: In the absence of any obvious intraoperative incident or difficulty, this probably represents a traction injury or compression without nerve interruption. Spontaneous recovery is considered possible.
Discovery of a secondary deficit during the recovery phase that does not follow the usual chronology: This is usually an observation made during rehabilitation and should be assessed in the context of the two previous situations described.

Nerve Injury Analysis

The evaluation of the neurological deficit is based upon clinical findings utilizing reference sensory-motor tests to locate the neurological lesion. A distinction is made between truncular lesions in which deficits are limited to the territory of a nerve (axillary, radial, musculocutaneous) and more extensive plexus lesions corresponding to the root level. Truncular lesions may result from all mechanisms of injury, whereas plexus or pluritruncular lesions are most often the result of stretching or compression mechanisms with intact neural continuity resulting in a better prognosis. In the initial phase, the ENMG is of little additional value, but radiographs and advanced imaging (computed tomography scan, ultrasound) are often necessary to search for a skeletal, hardware/implant, cement extrusion, or hematoma as a cause of the deficit.

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