Management of Adult Brachial Plexus Injuries

Published on 13/03/2015 by admin

Filed under Neurosurgery

Last modified 13/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1375 times

Chapter 197 Management of Adult Brachial Plexus Injuries

Brachial plexus injuries comprise approximately one third of all peripheral nerve injuries and are seen in just more than 1% of patients presenting to a trauma facility.1 They usually affect younger patients, with a median age of 34.2 Because of the association of such injuries with violent trauma and contact sports, males are affected more frequently than females. By the same line of reasoning, they are also often associated with injuries in other organ systems that are life-threatening. It was estimated that as many as 80% of patients with severe traumatic brachial plexopathy had multiple trauma to the head and skeletal system.3 Hence, there can be a delay in the diagnosis and treatment of brachial plexus injuries while the management of the other injuries are given priority.

The brachial plexus can be injured in several ways. The most common etiology is trauma, which can result in open or closed injuries. Among the closed injuries, the most common is caused by stretch or contusion, usually secondary to motor vehicular accidents involving motorcycles.4 Sports such as football, cycling, and skiing, among others, can also cause such injuries. Regardless of the setting, the mechanism is the same: the head and neck are usually forcefully pushed in one direction and the shoulder and arm in another. This results in severe stretching of the soft tissues, including the plexal elements and less frequently, the blood vessels.4 As for open injuries, the common etiologies are gunshot wounds and lacerations with knives or glass. Iatrogenic injuries may be open or closed. Nontraumatic causes of brachial plexus injuries include thoracic outlet syndrome and nerve sheath tumors, which cause injury by compression of plexal elements. In a survey of 1019 brachial plexus lesions by Kim et al.,2 the most common type of brachial plexus injury was due to stretch or contusion (50%), followed by thoracic outlet syndrome (16%) and nerve sheath tumors (16%). Gunshot wounds (12%) and lacerations (7%) complete the list. Because the majority of brachial plexus injuries are due to stretch/contusion, this chapter will focus on the diagnosis and management of such injuries.

Injury patterns can also be classified into supraclavicular and infraclavicular injuries. The supraclavicular plexus refers to the C5–T1 spinal nerves and the upper, middle, and lower trunks with their branches and divisions. On the other hand, the infraclavicular plexus refers to the cords and the nerves. In the series reported by Kim,2 72% of brachial plexus stretch injuries are supraclavicular, while 28% are infraclavicular. Of the supraclavicular injuries, C5–T1 palsy is the most frequent injury pattern, followed by C5–C7 then C5–C6. In terms of spontaneous recovery rate, C5–C6 has the best prognosis, with 30% of patients regaining significant function by 3 to 4 months. This compares favorably with C5–C7 palsy where approximately 16% recover spontaneously in the early months, and C5–T1 (pan-plexus palsies) with only 4% incidence of spontaneous recovery.4

Supraclavicular plexus injuries are more likely (52%) to come to surgery due to the severity of these injuries, with up to two thirds having avulsion of at least one spinal nerve.1 The infraclavicular lesions are less likely (17%) to be operated on, with half sustaining only neurapraxic injuries. Of the supraclavicular plexus injuries requiring surgery due to the lack of clinical recovery, two thirds will have at least some involvement of lower plexal (C8 and T1 spinal nerve) elements. The majority of these with pan-plexal involvement will have avulsed one or more spinal nerves, and exceedingly few will regain any useful function without intervention. On the contrary, when lower plexal elements are spared, and the primary injury thus less extensive, up to 25% may still make a good functional recovery of involved elements after neurolysis alone, without nerve repair.4

Surgical Anatomy

The brachial plexus originates at the level of the spine and usually includes the C5, C6, C7, C8, and Tl spinal nerves, the three trunks of the plexus, and their anterior and posterior divisions (Fig. 197-1A). Spinal nerves and trunks are supraclavicular, whereas divisions tend to lie behind the clavicle. Lateral, posterior, and medial cords are infraclavicular, as are their origins for the major nerves of the upper extremity (Fig. 197-1B).

Spinal Nerves

Each individual spinal nerve or root of the plexus originates as multiple sensory rootlets from the dorsal root entry zone of the posterolateral sector of the spinal cord and usually as one ventral or motor rootlet from the ventrolateral portion of the cord. The dorsal rootlets combine to form one dorsal root per spinal segment before entering the foramen. Within the foramen, the course of the roots varies between 10 and 16 mm. The dorsal root ganglion is located at an intraforaminal level and usually at its midpoint. Shortly distal to this, the anterior and posterior roots blend together to form the (mixed) spinal nerve. Posterior primary branches or rami then go to the paraspinal muscles and the much larger anterior ramus contributes to the brachial plexus.

Within the foramen, the C5 spinal nerve gives rise to a dorsal scapular nerve branch, which supplies the rhomboids. In addition, a branch that contributes to the long thoracic nerve exits the foramen posterior to the spinal nerve. The C4 spinal nerve may also make a small contribution to the plexus. Rarely, this may be substantial and thus represent a prefixed plexus. C6 blends with C5 to form the upper trunk. Usually, the long thoracic nerve arises from the dorsal surface of the distal portion of C6, just before it melds into the upper trunk. The C7 spinal nerve blends imperceptibly into the middle trunk with little to differentiate the two. C8 combines with Tl to form the lower trunk. It is at this level that rami communicantes are most likely seen coming and going from spinal nerve. These rami and their ganglia form the cervical sympathetic chain, whose largest ganglion is usually found posterior to the vertebral artery close to the latter’s division from the subclavian artery. Occasionally, T2 or a contribution from it may combine with T1 or its junction with the lower trunk to help form the latter.

Trunks

The upper and middle trunks are the most readily identified portions of the supraclavicular plexus. The upper trunk is usually adherent to and sometimes partially covered by the anterior scalene muscle. As one proceeds distally along the lateral edge of the trunk, the suprascapular nerve is encountered arising from the dorsolateral surface of the distal upper trunk, just as it forms anterior and posterior divisions. This trident-like structure, with suprascapular nerve, posterior and anterior divisions (from lateral to medial) is an excellent landmark for the termination of the upper trunk (Fig. 197-1A).

The middle trunk is found beneath the anterior scalene and is often covered by some muscular connections between the anterior and medial scalene or with scar tissue resulting from injury. It is usually smaller in caliber than either the upper or lower trunk. The posterior division of the middle trunk combines with its counterpart from the upper and lower trunks to form the posterior cord deep and just distal to the clavicle. The middle trunk anterior division combines with that from the upper trunk to form the lateral cord.

The lower trunk is usually relatively short and lies somewhat behind the subclavian artery. Exposure is aided by skeletonizing the inferior surface of the subclavian artery so that it can be gently elevated by a vein retractor. The posterior division of the lower trunk blends with the corresponding divisions from the other trunks to help form the posterior cord. The bulk of the lower trunk proceeds directly through its anterior division to form the medial cord.

Divisions

Although each trunk has an anterior and a posterior division as outlined above, they can blend with other divisions before forming cords. Sometimes one or more divisions trade bundles of nerve fibers back and forth several times.5 In addition, the site at which cords begin distal to the clavicle can vary from patient to patient. Separating divisions in cases in which there has been a stretch injury, gunshot wound, or prior vascular dissection can be quite difficult. The surgeon works from trunks in a distal direction and cords in a proximal one to expose the divisions.

Cords

These are named, by convention, in relation to the axillary artery at the level of pectoralis minor. The lateral cord is usually superficial to the artery and is the first major neural element encountered after section of the pectoralis minor muscle as one begins dissection in the infra-clavicular region. It terminates in a contribution to the median nerve and an oblique takeoff running laterally to form the musculocutaneous nerve (Fig. 197-1B). The latter dives immediately between the two heads of the biceps muscle but usually gives off one or more coracobrachialis branches first.

The posterior cord is deep or posterior to axillary artery. Several subscapular branches (upper and lower) usually arise from the posterior cord and run inferiorly and obliquely. A relatively sizable branch, the thoracodorsal, runs from its posterior aspect almost directly posteriorly to supply the latissimus dorsi. The cord then divides into its two major branches, the axillary and the radial nerves. After coursing inferiorly and slightly laterally, the axillary nerve dives down to reach the quadrilateral space and eventually the deltoid muscle in the posterior arm. The major posterior cord outflow is the radial nerve, which runs inferiorly towards the humeral groove to wind around the humerus. A very important anatomic landmark is the medial relation between the radial nerve and the profundus branch of the axillary artery. This can be used to locate the proximal radial and differentiate it from the more lateral axillary nerve.6

The medial cord sends a major contribution to the median nerve which wraps around the medial and superior side of the axillary artery. As this contribution is given off, so are the ones to the ulnar nerve and the medial brachial and antebrachial branches. These neural structures remain medial to the brachial artery as they begin their descent down the arm. Be aware that stretch injury can change the positions of trunks, cords, and nerves and their proximal to distal positions in relation to the usual anatomic landmarks of the arm.

Diagnosis

History and Physical Examination

It is important to obtain a good clinical history with regard to the mechanism of injury and the deficits incurred. Generally, a high-velocity motor vehicular accident would result in a higher risk of root avulsion. The evolution, or lack thereof, of the patient’s motor and sensory symptoms over time is extremely helpful. Worsening of the symptoms may indicate an ongoing compressive lesion such as a hematoma, whereas improvement over time suggests spontaneous recovery and possibly, nonoperative management. Other accompanying injuries, specifically vascular and musculoskeletal, along with any surgical intervention performed for these, must be elicited by the examiner.

A comprehensive physical examination begins with inspection. Typical positioning of the limb suggests involvement of the upper or lower plexus elements or both. For example, upper plexus palsy (Erb’s palsy) has the characteristic “waiter’s tip” position, a lower plexus palsy (Klumpke’s palsy) typically results in a “claw hand,” and a pan-plexus palsy usually results in a flail arm. One then proceeds to perform an assessment of the shoulders, neck, and high back from behind with the patient standing. One can readily spot asymmetry of the shoulder girdles, dropped shoulder, or laterally rotated scapula. In addition, the parascapular area is inspected for rhomboid atrophy, winging of the scapula, or atrophy of supraspinatus, infraspinatus, or deltoid muscles. Muscular atrophy can be a true neurogenic type secondary to muscle denervation, or at times from disuse. The mechanics of shoulder abduction and internal and external rotation of the upper arm should be viewed from behind, as can the response of latissimus dorsi to a deep cough.7 If there is a question of diaphragmatic paralysis, the chest can be percussed from behind, matching inspiratory tympani with that on expiration. Then, standing at the patient’s side, one can recheck internal and external rotation of the arm as well as adduction of the arm by the pectoralis and other muscles. Biceps/brachialis and brachioradialis can then be tested as elbow flexors and triceps as an elbow extensor. With the elbow fully extended, pronation and supination are tested, followed by wrist extension and flexion.

Hand muscle function is best tested with both the subject and the examiner seated and facing each other. The patient’s hands can be placed palm up on the knees for finger flexion testing and palm down on the knees or on a flat surface to test for extension. Each hand can then be held and manipulated to test for fine muscle hand intrinsic function, presence or absence of sweating, and sensory testing. For motor testing, the British Medical Research Council (MRC) grading system (0–5) is most commonly used.

After inspecting and testing these muscles, the examiner’s attention is directed to the front of the patient’s body. The neck is also inspected and palpated. Associated findings such as Horner’s syndrome should be looked for. Scars in supraclavicular, infraclavicular, and axillary spaces should be inspected and palpated. Deep tendon reflexes are ascertained and compared to the contralateral extremity, followed by a sensory exam.

Patterns of Injury

On presentation, an attempt is made to localize the injury to the involved plexus elements based on the history and physical examination, supplemented by electrodiagnostic and imaging investigations. During assessment, functional loss of each element is graded as complete, incomplete or none. Generally, the clinical deficits with truncal, cord, and cord-to-nerve level injuries are relatively constant, the exception being the wrist and finger function that remain after combined middle and lower trunk damage. In addition, lower trunk loss sometimes involves more than hand intrinsic muscle and ulnar distribution sensory loss.7 C7 injuries can result in surprisingly few deficits, often only partial triceps weakness, as other spinal nerves carry input to the muscles supplied by this element. At the division level, injuries can have different patterns of loss, depending on which truncal outflows are involved and the proportion of anterior and posterior division loss. The typical motor and sensory involvement for each spinal nerve and truncal element are summarized in Table 197-1.

TABLE 197-1 Plexus Element Injured and Respective Distribution of Motor Deficit

Structure Involved Distribution of Loss
C5 Supra- and infraspinatus, deltoid; rhomboids and serratus anterior also if injury is very proximal
C6 Biceps, brachialis, brachioradialis, supinator
C7 Triceps, pronator teres, some latissimus dorsi
C8 Wrist and finger flexors, finger and thumb extensors, some hand intrinsics
T1 Hand intrinsics
Upper trunk (C5–6) Supra- and infraspinatus, deltoid, biceps and brachialis, brachioradialis, supinator
Middle trunk Same as C7
Lower trunk (C8–T1) All hand intrinsics, some wrist and finger flexor and extensor loss

Case Illustration: Diagnosis

A 56-year-old, right-handed man was involved in a motorcycle accident and dislocated his right shoulder joint. He noticed numbness of his radial three fingers and was unable to abduct his shoulder or flex his elbow. Initially he also had difficulty extending his wrist, fingers, and elbow. His shoulder dislocation was reduced, and he was evaluated by a neurosurgeon 6 weeks later. Atrophy of his deltoid and biceps muscles was evident. No contraction of his deltoid, supraspinatus, infraspinatus, biceps, or brachioradialis muscles could be appreciated, but his elbow, wrist, and finger extension had recovered to MRC grade 4. His wrist and finger flexors and hand intrinsic muscles functioned normally. Clinically, he presented with Erb’s palsy. Electrodiagnostic studies confirmed denervation of his biceps, deltoid, and supraspinatus muscles with reduced activation of triceps and pronator teres. Positive radial nerve sensory nerve action potentials (SNAPs) were recorded with stimulation at his insensate thumb, suggestive of a preganglionic lesion.

Four months after the injury, there was still no sign of deltoid, supraspinatus, or biceps contraction, but his elbow, wrist, and finger extension strength had returned to close to normal. A magnetic resonance image (MRI) study of his cervical spine demonstrated the appearance of a pseudomeningocele at the C4/C5 level on the right side and asymmetry of the rootlets, suggestive of a proximal injury to the C5 spinal nerve.

Five months postinjury, he underwent right brachial plexus exploration and was found to have a preganglionic injury at C5 and C6, indicative of avulsion injury. Nerve transfers (accessory to suprascapular nerve, triceps branch to axillary nerve, and ulnar fascicle to biceps branch of musculocutaneous nerve) were performed in an attempt to restore the patient’s shoulder abduction and elbow flexion.

Diagnosis: Electrical and Imaging Studies

Preoperative Electrical Studies of Brachial Plexus Lesions

Although a thorough physical examination is paramount, well-selected electrical and imaging studies play an important role in the assessment of brachial plexus lesions.

Sensory Nerve Action Potential Recording

Presence of a SNAP recorded at skin level along the dipole of a peripheral nerve such as ulnar, median, or radial, providing clinical loss is complete in the distribution of the nerve stimulated, suggests preganglionic injury of one or more dorsal roots.9 This means that one or more dorsal roots feeding the nerve have been injured between the dorsal root ganglion and the spinal cord. Injury at this site does not lead to Wallerian degeneration of the ganglion’s more distal afferent fibers, so the nerve is still capable of conducting electrical impulses even if there is no central connection.

Even though the presence of a SNAP in the distribution of a nerve with complete clinical loss strongly implies a preganglionic injury, the absence of a SNAP in the distribution of a nerve with plexus dorsal root input does not exclude preganglionic injury. If an injury is extensive enough, as frequently happens, it damages both the pre- and post-ganglionic segments of the spinal nerve. In these cases, the sensory fibers do degenerate, and no SNAP is recorded even though root-level damage extends close to the spinal cord.10 Moreover, electrical evidence of preganglionic injury to the dorsal root does not guarantee that the ventral root is damaged as severely and as closely to the spinal cord, although it does strongly suggest it.11

Imaging Studies of Brachial Plexus Injuries

Angiography and Venography

These studies are probably done more often than is needed in the management of plexus palsies.11 Even so, we cannot be too critical of their use, particularly if penetrating injuries involving upper arm, shoulder, or neck are present. Angiography is certainly indicated if there is absence of a radial or carotid pulse, an expanding mass in the area of the wound, or presence of a bruit or a thrill in the area of the wound. Less often, arteriography is indicated for vascular injury associated with stretch/contusion.6,13 Associated vascular injury, especially if it involves the subclavian artery, denotes a particularly severe stretch injury to the plexus.1 This is because the blunt or stretch injury involving vessels as well as the plexus has severely distracted the shoulder and arm, resulting in a lengthy and proximal neural injury. This makes the probability of direct repair of a significant portion of the plexus lesion less likely than in one without vascular injury, but it does not completely exclude repair as a possible treatment option (Table 197-2).

TABLE 197-2 Relative Contraindications for Exploration and Direct Repair of Adult Plexus Stretch Injuries

Evidence of proximal spinal nerve injury at multiple levels, especially the upper levels; included is extensive paraspinal denervation by electromyogram, as well as rhomboid, serratus anterior, or diaphragmatic paralysis
Presence of sensory nerve action potentials elicited by stimulation of and recording from multiple peripheral nerves (median, radial and ulnar), whose sensory domain is anesthetic
Presence of pseudomeningoceles at multiple spinal nerve levels, especially the upper levels
Presence of extensive fractures of the cervical spine or serious cervical myelopathy
Injury limited to the C8–T1 spinal nerves or their outflows
Referral of the patient 1 year or more after injury
Cases in which there has been severe scapular or thoracic distraction, especially if there has been subclavian artery avulsion

Myelography and CT Myelography

Imaging studies such as myelography, CT, and MRI determine the location and severity of brachial plexus injuries and aid in treatment planning. Standard myelography (Fig. 197-2) is used to detect nerve root avulsions, and the addition of CT scan has increased its positive predictive value to more than 95%.14

Buy Membership for Neurosurgery Category to continue reading. Learn more here