A peripheral nerve injury can be classified in several ways. Historically, the first classification system by Sir Herbert Seddon (1943) was based on gross and histologic anatomical changes rather than mechanism of injury.¹ He described three types of nerve injuries. Firstly, neurapraxia involves a local conduction block at a discrete area along the course of the nerve. Wallerian degeneration does not occur and the recovery is excellent. Secondly, axonotmesis implies direct axonal damage, while thirdly, neurotmesis is the transection of a peripheral nerve. In both axonetmesis and neurotmesis, wallerian degeneration occurs distal to the site of injury; however while the former recovers, the latter does not. Within axonotemesis, Seddon described a degree of injury associated with scarring and less complete recovery. Within neurotmesis he described an “in continuity,” total scar, and no recovery injury. However it was Sunderland who expanded upon the earlier Seddon classification and emphasized five degrees of nerve injury.² Mackinnon later went on to include a sixth (Table 22.1).^3,⁴ First-degree (neurapraxia) and second-degree (axonotmesis) injuries recover spontaneously, the latter at the classic rate of 1 inch (2.5 cm)/month or 1–1.5 mm/day.⁵ Fourth- and fifth-degree injuries do not recover, while third- and sixth-degree injuries recover partially for different reasons. The difficulty with surgical correction of a sixth-degree injury is limiting the repair to the fascicles affected by fourth- and fifth-degree damage and not damaging fascicles with the potential for spontaneous recovery.

Table 22.1 Classification of nerve injury

Nerve injuries can also be grouped by mechanism of injury and whether they are open or closed. This clinical classification is useful in evaluating nerve injuries, determining the likelihood for spontaneous recovery, and provides an algorithm for managing these injuries. Table 22.2 lists the typical nerve injury patterns and their significance with respect to assessment and treatment. For simplicity, nerve injuries can be grouped as: (1) penetrating injuries; (2) crush and compression injuries; and (3) stretch and avulsion injuries. While generally, avulsion and crush injuries tend to be closed injuries, they may be open. This implies a more severe force, is associated with soft-tissue, vascular, and orthopedic injuries and the extent of muscle and skin damage will ultimately influence the outcome of the nerve repair. More extensive soft-tissue and/or bony injuries raise the complexity as well as the likelihood for a staged reconstruction. Often, the nerve reconstruction is delayed in light of more acute vascular and orthopedic injuries.

Table 22.2 Classification of nerve injury by mechanism. The significance of each type of injury in terms of ability to repair and outcome is discussed

Type	May be injured	Significance
Stretch/avulsion injury
Avulsion	Nerve roots	Unable to be repaired primarily
	Nerves exiting	Indication for nerve transfer
	Foramen, bony fracture
Stretch	Any nerve	Mixed nerve injury (degree VI)
Crush and compression injury
Injury
Complex crush	Skin, subcutaneous	Varying degree of depth, loss of function is related to amount of tissue destruction
	Tissue, muscle, nerve, ± bone
Chronic compression	Nerve	Slow onset, reversible
Acute compression	Nerve ± muscle	Quick onset, reversible muscle ischemia, variable recovery of both muscle and nerve
Compartment syndrome	Nerve + muscle	Quick onset, reversible muscle ischemia if ischemia less than 6 hours; no or variable recovery of muscle if released after 6 hours
Penetrating injury
Sharp	Skin, subcutaneous tissue, muscle, nerve ± bone	Needs surgical exploration because of high probability of nerve severance
	All levels
Blunt	Variable	Injury may extend further than expected
Blast	Variable	Injury pattern depends on ballistic makeup and velocity
Electrical	Variable	Neuropathy is from damage to myelin sheath and ranges from neuropathy to causalgia

Penetrating injuries

Penetrating trauma can be a result of sharp or blunt penetration, and will often have concomitant vascular structures and tendons injured in addition to the nerve. A sharp laceration, such as a hand laceration from a knife or piece of glass, will almost always necessitate exploration if a nerve deficit is present: the likelihood that the nerve is partially or completely transected is high. It is recommended to explore these injuries semielectively within the first week. The further from the time of injury, the less likely the two ends of the nerve can be mobilized enough to coapt primarily and the more likely a nerve graft will be needed to overcome a gap. In our practice, however, acute nerve grafting is frequently performed if there is concern about a degree of injury that would make it difficult to reoperate in the future. In the event of a penetrating trauma with an associated vascular injury, immediate exploration is warranted. Occasionally in proximal injuries with large arterial injuries with or without underlying fractures, the nerve injury is overlooked in the face of more urgent vascular and orthopedic injuries. Rather, the deficit is noticed postoperatively, when it is unclear if the nerve injury is from the inciting event, iatrogenic during the repair of the vascular injury, or secondary to edema or hematoma. While a computed tomography scan or magnetic resonance imaging may be helpful to evaluate for the latter, internal scarring of the nerve may not always be clearly determined.

Blunt penetrating and blast injuries are usually treated conservatively, similar to closed crush and stretch injuries, because they are may recover spontaneously. The local-tissue edema often causes a neurapraxia that resolves; however, those that do not recover after 3 months should be evaluated by electrodiagnostic studies and the algorithm for traction or crush injury followed (Fig. 22.1).

Fig. 22.1 Algorithm for penetrating injury and lacerations. EMG, electromyogram; MRI, magnetic resonance imaging; CT, computed tomography.

Crush injuries

Crush injuries comprise the most common peripheral nerve injuries to the extremity. External compression may be complicated by increased internal pressure from hematomas, fractures, and local tissue edema. When minor, this may cause a temporary neurapraxia, but with greater compression, the likelihood of a permanent injury increases. The most severe consequence of a crush injury is the progression to compartment syndrome, which is a surgical emergency. Often an early sign of impending compartment syndrome is a decrease in vibration sensibility.⁶ Compartment syndrome is discussed in greater detail in another chapter.

While nerves are fairly resistant to injury, especially when the surrounding tissue is not significantly damaged, a mixed nerve injury can often occur. A more extensive crush injury can cause local tissue damage that contributes more to the loss of function than the nerve injury. Muscle tissue is the most susceptible to external forces. Even if the injury is not significant enough to cause a compartment syndrome, the local destruction of muscle may lead to muscle death. Tendon and skin are more resistant and can withstand higher compressive forces before irreversible damage to the cells results.

The nerve portion of the injury is usually treated conservatively and exploration is warranted if the nerve recovery does not follow an expected pattern. Along with avulsion injuries, the algorithm is to follow recovery for 3–4 months and intervene if the expected recovery does not appear to be forthcoming (Fig. 22.2).

Fig. 22.2 Algorithm for closed traction, stretch, and avulsion injuries. EMG, electromyogram; MUPs or nascent units.

Stretch and nerve avulsion injuries

Stretch injuries occur because the strain on the nerve exceeds the maximum limit and the internal structure of the nerve becomes injured without any appreciable external evidence of injury.

Nerves that are stretched to the point of avulsing from the proximal end suggest a high-velocity or high-impact injury that is often associated with limb-threatening injuries that take precedence over the nerve injury. The nerves tend to be avulsed around areas of tethering, such as bony foramina and the spinal cord. If the proximal nerve can be accessed, as in injuries of the obturator nerve in the pelvis, a graft can be placed through the orifice and a neurorrhaphy with nerve graft may be performed. For areas such as the cranial nerves or the spinal roots, where the portion proximal to the avulsion is either central nervous tissue or inaccessible due to skeletal constraints, reconstruction is done via nerve transfers.⁷ Our current surgical algorithm focuses on nerve reconstruction first, followed by tendon transfers and associated procedures to augment or complement the nerve reconstruction when warranted (Fig. 22.2).⁸

Nerves avulsed at the neuromuscular junction present a different problem, as the distal end is unavailable. In the case of motor nerves that are avulsed from the muscle bellies, implantation of the proximal nerve directly into the muscle is the alternative when no distal end is available. Some studies show as good as M4 motor recovery 1–2 years after direct nerve to muscle neurotization ⁹; however, experimental studies do not support these findings; rather, recovery is much less than a nerve coaptation would produce.¹⁰

Hint: Sharp injuries with acute nerve deficit should be explored early (within 1 week) in order to be able to perform a primary neurorrhaphy. Crush and traction injuries should be treated conservatively with serial exams and electromyograms (EMGs) at 3 months if no clinical evidence of recovery is noted.

Evaluation of nerve injuries

A thorough physical exam remains the most reliable method for determining the neurologic defect. Sensation, or lack thereof, can be tested using Semmes–Weinstein filaments, two-point static and moving discrimination, or the “ten test.” The quick and easy ten test sensory exam uses the patient’s own subjective perception to moving light touch in order to elicit differences in sensation.¹¹ For example, to test for a median nerve injury, both the injured and uninjured index fingers of the patient are touched at the same time over corresponding areas of each finger and the patient is asked if the subjective sensation is the same or different. This technique is particularly useful in young children who may not be able to cooperate with a two-point discrimination test.

In patients who present with an acute motor deficit or palsy, determining if the nerve will recover spontaneously or if surgical intervention is needed can often be difficult. The mechanism of the injury can often assist in the preoperative evaluation. Any sharp penetrating injury with no clinical evidence of recovery should be explored. Optimal timing is 0–7 days, as long as the patient is surgically stable and a skilled surgical team is available. Any injury where there is a high index of suspicion of nerve transection should be explored and repaired. The advantage of repair within the first 2 weeks of injury is that at this early time point the nerve ends have not retracted and primary neurorrhaphy is often possible.

Closed traction injuries, partial avulsion, and crush injuries with palsy are more difficult to evaluate. Waiting 3–4 months with serial physical examinations to assess for evidence of spontaneous recovery is recommended. At 3 months, electrodiagnostic testing is advised when no clinical recovery is evident as EMG changes precede clinical recovery. If there is no evidence of reinnervation occurring by 3 months (e.g., motor unit potentials), surgical exploration and reconstruction are warranted.

There are clinical investigations using newer ultrasound machines that can detect digital nerve neuromas; however these studies are still investigational and are highly operator-dependent.

Hints: We prefer to evaluate the patient early and follow the clinical exam, as well as ordering electrodiagnostic testing, in order to minimize delay in recognizing a nerve deficit that will not resolve spontaneously.

Nerve repair

Timing of repair

When there is a high index of suspicion that a nerve transection exists, there is no reason to wait as long as the patient is clinically stable and able to be taken to the operating room for exploration and repair of the nerve. Nerves repaired acutely within the first 2 days are considered repaired primarily. A delayed primary repair occurs between 2 and 7 days. In either case, the proximal and distal ends of the nerve are freshened and an end-to-end coaptation performed. Nerves repaired after the first week are considered repaired secondarily. Clearly these cut-off days of 2 and 7 are arbitrary numbers. Often even at 2–3 weeks from injury, the nerve can be coapted without need for a graft; however, the longer the time from injury, the less likely that a primary neurorrhaphy can be achieved, even with significant mobilization of the proximal and distal nerve ends.

Tension and nerve repair

Excessive tension across a nerve repair is known to increase the scarring at the coaptation site and impair regeneration. In an uninjured nerve, a 15% strain of the nerve causes a reduction in microvascular flow and, for an hour after relaxation, a delay of peak velocity to 66% of initial value persists.¹² Mild tension, on the other hand, is actually believed to be beneficial to the repair by stimulating neurotropic growth factors.

In clinical practice we do not formally measure the tension across a neurorrhaphy; however we always avoid tension on a repair. The two ends of a nerve are mobilized in order to bring the ends in reasonable approximation. Strain on the nerve decreases the microcirculation and excessive tension will cause the repair to break down. In addition, tricks such as positioning the arm in adduction or placing the wrist and fingers in flexion will significantly decrease the tension across the repair depending on the location of the injury and may increase the total length of available nerve; however, we recommend avoiding postural manipulation in order to force primary repair. Not only can dehiscence occur when the joint near the repair is moved too early, but it may create significant stiffness from prolonged immobilization.¹³ An immobilized nerve also results in scarring at the repair site.

Type of repair: epineural versus fascicular

Any repair that withstands gentle range of motion is considered a “tension-free” repair. Giddins et al.¹⁴ showed in a cadaveric study comparing suture size to the strength of an acute repair of the median nerve that 9–0 nylon withstood the greatest distractive forces. At a lower tension 10–0 snapped, and 8–0 sutures pulled out of the nerve tissue. However, in clinical practice, 10–0 and 8–0 sutures are often used based on the size of the nerve, the thickness of the epineurium, and the amount of inflammation.

Alternatively some surgeons use fibrin glue, especially when there is no tension in the repair. Laser energy for epineurial coaptation has been investigated experimentally; however it produces heat that damages nerve tissue and results in unacceptably decreased tensile strength at the repair site. The gold standard remains microsuture applied under microscope control.

Epineural repair is the preferred method of repair once the severed ends are freshened surgically. External markers such as a vessel on the surface and matching the fascicular patterns are used to align the fascicles without overlapping (Fig. 22.3). For major peripheral nerves, an argument for perineural repair can be made to improve alignment of the larger fascicular groups individually; however, clinical studies support both techniques as equally effective as long as the fascicles were not overlapped (Fig. 22.4).¹⁵ The disadvantage of a perineural repair is that the extensive dissection and the permanent intraneural stitches can lead to increase fibrosis.¹⁶ In practice, it is often difficult to align the fascicles accurately, as trauma, edema, and scarring can distort the normal topography.