Principles of peripheral nerve surgery

Structure of the peripheral nerve trunk

The anatomy of a peripheral nerve trunk is shown in Fig. 34.1. Nerve impulses are conducted by axons. The nerve contains many axons which are supported by connective tissue structures. Neurons consist of a cell body, associated dendrites and usually one axon. In order to remain viable an axon must be connected to its cell body. All axons are sur­rounded by Schwann cells. In myelinated fibres the Schwann cells form an insulating sheath, each Schwann cell being asso­ciated with only one axon. Integrity of the myelin sheath is necessary for conduction of nerve impulses in myelinated fibres. Unmyelinated fibres are composed of several axons wrapped by a single Schwann cell. The Schwann cell base­ment membrane, together with endoneurial collagen fibres, forms the endoneurial tube. Large numbers of nerve fibres are gathered in fascicles surrounded by a connective tissue sheath called the perineurium. The fascicles are bound together and the whole trunk ensheathed by a further con­nective tissue layer called the eprneurtum.

Response of a nerve to injury

If trauma to a nerve is sufficient to disrupt axons then the distal part of the nerve undergoes Wallerian degeneration. In this process there is lysis of the axoplasm and fragmentation of myelin sheaths leaving an endoneurial tube containing Schwann cells. The axons in the proximal part of the nerve have the potential to regenerate into the endoneurial tubes of the distal segment and subsequently make connections with target organs. The regeneration proceeds slowly with axons growing at only 1—2 mm/day in humans. The extent of dam­age to the supporting connective tissue layers influences the quality of recovery and is, hence, the basis of the classifica­tion of nerve injuries.

Classification of nerve injuries

The most widely used classification of nerve injuries in the UK was described by Seddon (1942) after study of a large number of battle casualties during World War II. There are three types of injury of increasing severity:

       neuropraxia;

       axonotmesis;

       neurotmesis.

Neuropraxia (nerve not working)

This is a local block to conduction of nerve impulses at a dis­crete area along the course of a nerve. The axons are in con­tinuity and therefore Wallerian degeneration does not occur. Nerve conduction distal to the site of injury remains normal. Experimental work suggests that the conduction block results from localised demyelination of fibres in the damaged seg­ment of nerve. Neuropraxia is a relatively mild injury typi­cally caused by moderate compression such as that caused by a tourniquet, slight stretching or the passage of a missile close to a nerve. Recovery is complete providing the cause is removed, but the time varies from days to several weeks.

Axonotmesis (axons divided)

This represents an anatomical disruption of the axons and their myelin sheaths. However, the supporting connective tissue structures including the endoneurial tubes, perineurl­um and epineurium are still intact. Wallerian degeneration occurs distal to the site of injury and, hence, distal conduc­tion is lost. Arxonotmesis results from a more severe blow or stretch injury to a nerve. For example, radial nerve palsy associated with fracture of the humerus is usually an axonotmesis. Recovery occurs by axon regeneration proceed­ing at a rate of 1—2 mm/day. Axons regenerate along the same endoneurial tube and therefore connect with the same end organ as before injury. The prognosis is good, restoring near-normal sensory and motor function.

Neurotmesis (whole nerve divided)

This is the state where the nerve has been completely severed or is so seriously disorganised that spontaneous recovery is not possible. The axons and the supporting connective tissue structures are disrupted, and Wallerian degeneration occurs distal to the site of injury. Typically neurotmesis occurs as a result of an open injury such as a stab wound but high-energy traction, injection of noxious drugs and ischaemia can also destroy a nerve in this way.

If appropriate surgical repair is carried out then recovery may occur by axonal regeneration at a rate of 1—2 mm/day. In contrast to axonotmesis, the quality of recovery is never per­fect after neurotmesis. This is probably the result of the failure of correct ‘rewiring’. Because the endoneurial tubes and other connective tissue structures have been disrupted, even with the best repair, regenerated nerve fibres connect with muscles or sensory organs which they did not previously innervate.

Sunderland’s classification

In 1951 Sunderland defined five degrees of nerve injury on the basis of increasing anatomical disruption of the nerve trunk (see Table 34.1). Although Seddon’s classification is simpler and more widely used in the UK, Sunderland’s classification is useful in its distinction between third- and fourth-degree injuries when exploring a damaged nerve. If the fascicles are in continuity (not worse than third-degree injury) then sponta­neous recovery is possible, whereas if the fascicles are disrupted (fourth-degree injury) then spontaneous recovery will not occur and immediate nerve grafting may be considered.

Injection injuries

Injection of toxic substances directly into a nerve leads to a very intense fibrotic reaction in the nerve. Immediate exploration, incision of the epineurium and irrigation of the nerve trunk is recommended, but the outcome is poor.                                 

Clinical features of nerve disorders

As with other medical and surgical problems, diagnosis of conditions affecting nerves is based upon history, examination and special investigations. In the case of trauma it is partic­ularly important to establish the mechanism. High-velocity and open injuries produce more severe nerve injuries.

The clinical findings on examination of patients with nerve injury include motor and sensory dysfunction but depend, in part, upon the grade of injury. With neurapraxia there is usually complete paralysis of the appropriate muscle groups but some sensation and autonomic function is preserved. In the case of axonotmesis and neurotmesis there is complete loss of muscle power, sensation and autonomic function. The latter is most easily shown by lack of sweating in the distribution of the nerve. This is a useful objective sign as it does not require a co-operative patient. The nerve injured and the level at which the injury has occurred can be worked out from a careful physical examination and knowledge of the anatomical distribution of the nerves. Nonetheless, there is significant crossover in sensory function and also in some motor function, particularly when considering nerve roots (Table 34.2 and Fig. 34.2).

It is useful to grade the level of dysfunction of nerves, partic­ularly in the assessment of recovery and the results of treat­ment. The system widely used is the 1975 update of the 1954 Medical Research Council (MRC) classification (Tables 34.3 and 34.4). This grading system is good, and widely used, but is still a rather coarse measure of muscle function and sensation.

  Clinical examination needs to be conducted with care, particularly with those patients who may have difficulty co-operating. The findings should be accurately documented. Two-point discrimination is particularly useful for assessing sensation in the hand as it is an objective measurement and normality (approximately 4 mm on the finger pulps) excludes significant nerve injury. If there is any doubt initial first aid should be carried out and the patient re-examined within 48 hours. Diagnosis can be difficult and severe nerve injuries are regularly missed.

Investigation

While the most important assessment of nerve pathology is undoubtedly clinical, useful additional information can sometimes be obtained from neurophysiological studies or imaging.

Neurophysiological investigations require complex stimu­lation and recording apparatus. Interpretation of the results requires experience and is reliant upon the skill of the neurophysiologist. There are two types of test available.

Nerve conduction studies these involve recording sensory or motor nerve action potentials and calculating the conduction velocity for given anatomical segments. Compression neuropathy can be identified by slowing of conduction.

       Electromyography (EMG) in this test muscle action potentials are recorded in response to voluntary activity. Denervation can be diagnosed and distinguished from reinnervation.

Using these tests it is possible to distinguish between a nerve injury where axons have not degenerated distal to the lesion (neurapraxia) and one were Wallerian degeneration has occurred (axonotmesis or neurotmesis). Axonotmesis and neurotmesis cannot be distinguished.

Magnetic resonance imaging (MRI) is showing some pro­mise in displaying peripheral nerve pathology and is likely to be used routinely in the future. Currently, its main appli­cation is in imaging cervical nerve roots after brachial plexus injuries.

Treatment

Open injuries

If there is clinical evidence of a nerve injury associated with a wound, then it should be assumed that the nerve is divided until proven otherwise.

Surgical exploration of the nerves is advisable, once life-threatening haemorrhage has been controlled and providing the general condition of the patient allows operation. In addition, wounds in areas where important nerves are vul­nerable to damage should be routinely explored even in the absence of obvious neurological deficit, for example the flexor compartment of the forearm. Early repair of any divided nerves should be performed if possible. Exploration should therefore be undertaken by a surgeon with appro­priate experience to carry out repair of nerves if necessary. If a vascular repair is required then nerve repair should nor­mally be carried out at the same time. If the injury is in a site which is difficult to expose surgically, for example the brachial plexus, then transfer to a specialist unit should be arranged as soon as possible.

Closed injuries

Management of closed injuries where nerves have been subjected to stretch or compression is more difficult because the severity of nerve injury may not be clear. Neurapraxia and axonotmesis will recover spontaneously providing the cause, for example compression, is removed. However, sur­gical repair of the nerve is necessary for there to be any chance of recovery after neurotmesis. Results are markedly better if this repair is carried out early after injury.

Exploration and repair of nerves may be combined with fixation of any associated skeletal injury. In cases of low-energy injury it is reasonable to observe the nerve injury initially, unless operation is being carried for fracture fixation in which case the opportunity should not be missed to con­firm nerve continuity. Cases managed nonoperatively should be followed up carefully. If there is clear evidence of recovery after 2—3 months then nonoperative management can continue. If not, then surgical exploration should be con­sidered without further delay. Neurophysiology may be helpful in making the decision in some cases as the tests may detect early recovery which is not evident clinically.

Surgical repair

The essence of a good surgical repair of a nerve is accurate coaptation of the nerve ends without tension in a healthy bed of tissue. At operation the nerve ends are exposed, carefully avoiding further injury. If there has been a clean division of a nerve, then little dissection is usually required and direct suture can be carried out. However, if the nerve ends are ragged or the disruption has been caused by blunt trauma, it is necessary to trim the nerve back to healthy tissue with bulging nerve bundles. In delayed repairs significant scarring and retraction of the nerve ends may have occurred and it is, again, important to trim the nerve back to normal tissue. In these circumstances there will be a gap between the nerve ends. In the past extensive mobilisation of some nerves was recommended to allow direct suture. However, it is seldom possible to get much length by this manoeuvre and the repair is invariably under tension. Therefore, if there a significant gap is present it is usually better to perform nerve grafting. Occasionally, when a nerve injury is combined with a frac­ture, bone shortening may be justified to allow direct nerve suture.

Timing of nerve repair

Early nerve repair provides the best chance of satisfactory recovery and should be carried out provided that a well-trained surgeon and suitable equipment are available. Occa­sionally, if a wound is very contaminated then primary nerve repair may not be appropriate. In most circumstances it is possible to carry out early repair if sufficient wound debridement is carried out and plastic surgical expertise is available to provide flap cover of soft-tissue defects. If primary repair is not carried out then it is useful to apply one or two nonabsorbable sutures, either to hold nerve ends together or to suture a nerve end to local soft tissue, thereby minimising retraction and aiding identification at later surgery.

Direct nerve suture

When repairing a nerve, a microscope should be used to aid accurate alignment of the nerve and placement of sutures, which range in the order of 6/0 for large nerves (such as the sciatic nerve), 8/0 for the median nerve in the forearm, and 9/0 or 10/0 for digital nerves. It is important to orientate the nerve ends with the correct rotation in order to minimise crossover during recovery. The pattern of nerve fascicles and surface blood vessels can be used as guides for alignment. Sutures are usually placed in the epineurium (epineurial repair). There is probably no advantage in performing interfascicular repair except at distal sites where the nerve is dividing into terminal branches. Sufficient sutures are inserted to provide epineurial cover for all nerve bundles (Fig. 34.3).

Nerve grafting

When direct nerve suture is not possible an interpositional nerve graft is necessary. This involves harvesting a length of an ‘expendable’ nerve trunk, such as the sural nerve or the medial cutaneous nerve of the forearm. These are long slender nerves which supply only small areas of sensation. The nerve graft is usually cut up so that a number of strands can be used to build up a similar thickness to that of the nerve trunk being repaired (cable grafting; Fig. 34.4).

Postoperative management

After wound closure, the limb is immobilised to minimise any tension on the suture line with appropriate flexion of proxi­mal and distal joints. These are held in a cast for a minimum of 3 weeks. It may then be appropriate progressively to extend the proximal and distal joints, thus gradually restor­ing normal tension to the nerves. After 6 weeks, free mobili­sation is permitted, assisted by appropriate physiotherapy.

Follow-up management

After nerve repair patients should have regular physiotherapy to maintain the passive range of movement in all joints prior to muscle recovery. In addition, patients should be monitored clinically to check that nerve recovery is occurring at the expected rate. Tinel’s sign is useful in monitoring axon regen­eration and should advance at about 1 mm/day. (Elicited by percussing over the course of the nerve, the patient feels tingling in the distribution of the nerve.) In the event of nerve recovery not progressing, then re-exploration of the nerve may be justified.

General factors affecting prognosis

The factors governing the prognosis of nerve repair are both general to all nerves and specific to certain nerves.

Age

Children recover much better than adults and this is probably the most important prognostic factor. Nonetheless, the secondary consequences of paralysis in children may be worse because of the associated growth abnormalities. Age over 50 years is a particularly poor prognostic factor for proximal nerve injuries.

The severity of in jury to the nerve

Seddon’s classification of nerve injuries relates the severity of injury to the prognosis. However, there are varying grades of neurotmesis which affect the chance of recovery after repair. A clean-cut nerve injury has the best prognosis, whereas high-energy injuries, such as high-velocity gunshot wounds or severe traction injuries, damage a greater length of nerve and have a much worse prognosis.

The level of in jury

In general, proximal lesions do worse than distal lesions although there do appear to be some exceptions to this rule.

The type of nerve

The classic teaching is that nerves with both sensory and motor fibres fare worse than pure sensory or motor nerves. The latter do not truly exist, as all motor nerves have some afferents from muscle spindles. However, it is certainly true that motor nerves to large muscle groups not requiring fine control have a better prognosis than motor nerves supplying the small muscles of the hand.

Associated injuries

Nerve repairs with associated vascular injuries, soft-tissue damage and fractures are less likely to heal with a satisfactory result. It is important that associated vessels and other structures are repaired as far as possible.

Delay

Early repair of nerves, that is within a few days of injury, gives the best results and is one of the main factors which the surgeon can influence.

Special types of nerve injury

Compression neuropathy

This is the term used to describe chronic dysfunction of a nerve as a result of local compression at some point along its course. Compression neuropathy is one of the most frequent single conditions presenting to orthopaedic and hand clinics. The most common sites of compression are the median nerve at the carpal tunnel and the ulnar nerve at the cubital tunnel or Guyon’s canal. These are anatomical sites where the nerve is surrounded by unyielding bone and ligaments. Sometimes there is an identifiable cause such as tenosynovitis within the carpal tunnel, but in many cases there is no obvious cause. Compression of a nerve has a direct effect on the myelin sheaths, as well as causing ischaemia of the nerve with con­sequent fibrosis. It also appears that damage results from loss of mobility of the nerve at the point of entrapment. The patient initially complains of pain and altered sensation in the distribution of the affected nerve. In more advanced cases there is loss of sensory and motor function. Most compres­sion neuropathies respond to surgical decompression of the affected nerve.

Irradiation

Radiation neuritis can occur up to 20 years after the radiation, the classic site being the infraclavicular brachial plexus following radiation for breast cancer. Fortunately, this is rare. Characteristically, there is severe pain with some motor and sensory changes. The pain is cry difficult to treat. Surgical exploration and release of nerves has been beneficial in some patients.

Pain

The pain following nerve injuries or other nerve pathology can be of the most severe intractable type, leading to requests for amputation and even depression and suicide. The cause of this pain is poorly understood. Local nonoperative treat­ment includes encouraging use and movement of the limb, and transcutaneous electrical nerve stimulation (TFNS~. This works as a counter-stimulus to the pain. In addition to simple systemic analgesics, medication to suppress nerve excitability, such as carbamazepine, and antidepressants, such as amitryptilline, can be useful. There are certain occasions where pain of nerve origin may be influenced by surgical intervention.

Cusalgia is pain as a result of an injury (often partial) to a major nerve. The pain typically has an intense burning character. This pain tends to improve with nerve recovery and therefore any surgical measures should be aimed at facilitating this. Sympathectomy may be helpful in resistant cases

Nerve compression may cause severe pain (neurostenalgia). Avulsion of spinal nerve roots from the spinal cord, for example with traction injuries to the brachial plexus. This is a complex pain syndrome involving damage to the spinal cord and loss of the normal afferent signals from the limb. Re-establishment of some neurological input is by nerve transfer. In the case of the brachial plexus intercostal nerve transfer may prove useful. Neuroma if a nerve is wholly or partially divided and not repaired, for example at amputation, then axons attempting to regenerate form a neuroma on the nerve end. The neuroma may he exquisitely sensitive to any pressure, particularly if it is tethered in scar tissue or situated at a prominent point. Surgery may be helpful to restore continuity of the nerve by repair or grafting, if possible, or to move a neuroma to a less prominent position

Reflex sympathetic dystrophy (algodystrophy) this is a specific syndrome which can occur after trauma or surgery where a cycle of pain and dysfunction is set up and leads to a chronic state associated with sympathetic over-activity. The limb involved becomes painful and tender to normal stimuli. This leads to disuse, stiffness and trophic changes. It is important to recognise the condition as early as possible and to break the vicious cycle. In addition to standard analgesics, guanathedine blockade to suppress sympathetic activity is useful to facilitate vigorous physiotherapy.