Nerve Repair and Grafting in the Upper Extremity

S. Houston Payne, Jr., MD

J South Orthop Assoc. 2001;10(2) 

In This Article

Treatment

The majority of peripheral nerve injuries are best treated by a thoughtful surgical reconstruction. However, nonoperative treatment is indicated in several circumstances. The first of these is injury to a sensory nerve innervating a noncritical area. In the digits, this would include the ulnar border of the ring finger and possibly the middle finger. After discussion with the patient concerning symptoms, functional needs, and realistic outcomes, other digital sensory areas may occasionally be considered noncritical. Other injuries, such as those to the cutaneous nerves of the forearm, may be treated nonoperatively if agreed on during careful discussion of options with the patient. It is important to emphasize patient involvement in the consideration of nonoperative treatment of peripheral nerve injury. Decreased sensation in an area that might seem trivial to one patient may be critical to another. In some situations (eg, after injury of the radial sensory nerve), nerve repair may be indicated primarily to reduce neuroma symptoms; in these cases, sensory return is a secondary goal.

Realistic expectations for recovery should be considered when discussing operative versus nonoperative treatment. Patient age, level of injury, mechanism of injury, and associated medical conditions all influence outcome and, in certain cases, may make repair or grafting unreasonable.

In discussing the timing of nerve repair, treatment is commonly described as primary or secondary. Primary nerve repair includes repairs carried out within 1 week of injury. Any repair carried out later is termed secondary.[40] The classification is, arguably, somewhat arbitrary, but a precise definition is extremely useful in discussion of results. Experimental evidence has shown very clearly that axons regenerate more quickly in the setting of secondary repair.[41] In spite of the experimental evidence, no clinical advantage has been shown with secondary repair. Primary suture under appropriate conditions has proven superior in animal models and in clinical series.[42,43,44,45] Primary repair is preferable, but situations may arise in which delayed suture is desirable.

Conceptually, nerve repair should result in the appropriately aligned coaptation of healthy fascicles in a well-vascularized tissue bed under minimal tension. If any of these goals cannot be achieved in the primary setting, secondary repair is more appropriate. For crush injury, the extent of neural injury cannot initially be accurately determined. Repair under these circumstances risks joining injured fascicles and thereby severely compromising the success of the repair. The condition of the patient in relation to either injury or associated medical conditions may preclude primary repair. Appropriate surgical equipment and adequately trained staff must be available. Every attempt should be made to ensure that the first nerve repair is carried out under the best possible conditions.

Nerve Repair

Epineural repair requires adequate exposure. Anesthesia should be selected to provide adequate time for careful exposure, assessment, mobilization, and repair. Use of a pneumatic tourniquet provides a bloodless field for dissection. Magnification with loupes or, more commonly, the operating microscope improves the technical quality of the repair and favorably affects outcome.[46] The nerve ends for repair are gently mobilized and cleared of soft tissue, which may obscure visualization of the epineurium at the repair site. Hemostasis is obtained with bipolar cautery. Careful note is made of external nerve markings, which may aid in appropriate orientation of the repair. In addition, inspection of the internal neural topography improves correct fascicular alignment. The nerve ends are then sharply transected perpendicular to the long axis. After transection, the nerve is carefully inspected with magnification to ensure that healthy-appearing, uninjured fascicles are exposed for the repair. Several sequential transections at short intervals (1 to 2 mm) may be necessary before the nerve endings are appropriate for repair. This step in the repair cannot be overemphasized. Failure to adequately resect injured tissue severely compromises the outcome of the repair. If this step results in a nerve gap so large that grafting becomes necessary, the surgeon should not hesitate to proceed with grafting instead of direct repair. Nerve grafting of uninjured nerve tissue over a short distance will provide results far superior to direct repair of injured neural tissue.

The repair is begun by placing two epineural sutures 180° to each other. Careful alignment is the critical factor in this first step. Observation of the repair during the first few minutes provides an interesting illustration of the speed with which the epineurium can be sealed simply from surface tension of local fluids. Therefore, additional sutures are placed sparingly. For a more detailed discussion of repair technique, the reader is referred to the full text of this chapter at www.orthotextbook.net.

To accomplish group fascicular repair, the initial exposure and mobilization of the nerve are the same as those described above for epineural repair. With the aid of an operating microscope, the nerve ends are inspected to identify fascicular groups amenable to individual repair. Matching fascicles are identified proximally and distally. The internal epineurium is then divided between fascicular groups. After mobilization is complete, the repair process is initiated to facilitate the repair -- in general, the least accessible fascicles, which are often farthest from the surgeon, are repaired first. Repair of the external epineurium may be helpful in alleviating tension during the repair. The internal epineurium is sutured with the fewest sutures necessary (commonly two) to oppose the fascicular group.

Individual fascicular repair requires isolation of individual fascicles. The fascicle is the smallest unit of nerve tissue that can be manipulated surgically. Interfascicular connections occur, and care must be taken to avoid injury during the dissection. The repair follows a pattern similar to that of group fascicular repair.

Sutureless Nerve Repair
Coaptation of nerve tissue without suture is appealing and would potentially eliminate the trauma associated with traditional suturing technique. The method has the potential to (1) be more efficient, (2) eliminate variables of tension due to suture placement and technique, and (3) improve alignment of fascicles. The two techniques that have been most carefully evaluated are coaptation by fibrin glue and by laser (see www.orthotextbook.net for additional information).

Fascicle-Matching Techniques
The more precisely axons are directed toward their appropriate end organ, the better the chance for successful nerve regeneration. Intraoperative nerve stimulation in the awake patient is a readily available tool that can aid in this goal. Hakstian[47] provided an early description of intraoperative nerve stimulation in 1968. The technique has been modified and improved over the years.[48,49,50,51] Patient response to stimulation of selected fascicles in the proximal nerve stump can differentiate motor and sensory groups. However, caution should be exercised. Awake stimulation requires a high degree of patient cooperation and is not tolerated by all patients. A thorough preoperative discussion, which outlines the proposed procedure and describes what the patient will experience, is crucial to the success of the procedure.

Histologic staining methods are available to identify motor and sensory fascicles in the divided nerve. Acetylcholinesterase is found in myelinated motor axons and in some unmyelinated axons, but not in myelinated sensory axons. Carbonic anhydrase is found in myelinated sensory axons. The detection of these enzymes with available staining techniques makes fascicle identification possible. Identification in the proximal nerve is possible indefinitely. Accurate staining in the distal stump is possible for about 9 days after nerve division.[52] The time required for intraoperative staining (about 1 hour) and the lack of clear evidence that the technique improves outcome have limited the use of this technique.[53]

Results of Nerve Repair
An accurate and reproducible evaluation of results after treatment is difficult. Multiple variables in injury, patient comorbidity, treatment, postoperative evaluation, and the reporting of results contribute to this difficulty. The most accurate information would be gained from a prospective standardized assessment. Even more difficult would be limiting each group to a certain age, injury type, specific nerve, level of injury, type of repair, postoperative protocol, and assessment. In spite of these difficulties, there is a great deal of useful information available regarding nerve repair and results.

The objective evaluation of motor and sensory recovery is essential to accurate assessment. The Medical Research Council provided a basis for the assessment of motor and sensory function after nerve injury using the relatively simple and reproducible system outlined in Tables 4 and 5 .[40,54]

The recovery of sensory perception is evaluated by static 2-PD, moving 2-PD, and pinprick. Static 2-PD is perceived primarily through the Merkel cell, which is slowly adapting and thus well-suited to continuous pressure. The Meissner corpuscle, a rapidly adapting receptor, fires at the beginning of a stimulus and then dissipates, making it more suitable for relaying information from moving 2-PD. Free nerve endings transmit painful stimuli, such as those from a pinprick. Dellon and Clayton[55] reported that moving 2-PD best correlates with a patient's ability to identify objects, and static 2-PD correlates with the time to identify objects. Both tests are needed to accurately assess functional sensation. Threshold density may be measured with 2-PD, and innervation density may be measured with monofilament testing.

Detailed information concerning outcome after peripheral nerve repair or grafting is beyond the scope of this review. For an expanded discussion, the reader is referred to the online chapter text (available at www.orthotextbook.net).

Nerve Grafting

Reconstruction after peripheral nerve injury may require management of segmental defects or "gaps" in the injured nerve. Local measures to overcome the problem include nerve mobilization, local joint positioning, nerve transposition, and bone shortening. Risks and benefits of each strategy must be carefully considered. Paramount to the decision-making process is the understanding that nerve repair under excess tension does poorly.[56] Nerve grafting is a readily available solution to the problem of excessive tension at the repair site. With the dependable outcomes after nerve grafting, extremes of joint positioning to accomplish end-to-end repair are not indicated.

Under ideal circumstances, the nerve graft will behave as the distal nerve stump would. Therefore, the graft must also undergo wallerian degeneration to provide a conduit for axon regeneration. Schwann cell survival in the graft is critical to this process. For the Schwann cells to survive, the graft must be appropriately revascularized. This process occurs both from the proximal and distal nerve stumps and from the surrounding tissue bed. In animal models, graft revascularization reaches supranormal levels in 4 to 5 days.[57,58,59] Initial revascularization occurs through the proximal and distal stumps and then the surrounding tissue. Ingrowth from local tissue creates extensive adhesions, which limit graft excursion. The first few days after grafting, cellular viability is dependent solely on diffusion from the tissue bed.[60] As graft size increases, central cellular necrosis occurs, because the volume of nerve tissue increases beyond the limits of perfusion or revascularization. This limitation contributes to poor outcome with trunk grafting.[61,62] Trunk grafts are now used uncommonly, unless harvested as vascularized nerve grafts.

Nerve Grafting Techniques
In group fascicular grafting, every attempt is made to accurately deliver regenerating axons through the graft material to a matching fascicular group in the distal stump. The distal nerve tissue may be marked and sent for histochemical staining, depending on clinical needs and laboratory capabilities. After graft harvest and careful hemostasis, grafts are sutured to individual fascicular groups with the minimally needed number of sutures. Emphasis again is placed on appropriate fascicular matching without tension.

Individual fascicular grafting is uncommon. A distal digital nerve defect is a specific, useful indication for individual fascicular grafting.[63] Other indications may arise when clinically critical single fascicles (eg, the thenar motor branch) can be identified.

Graft Material
Autogenous nerve graft is the most commonly used material for bridging nerve gaps. Ideally, the donor nerve provides a suitable environment for regeneration and results in acceptable donor morbidity. The sural nerve meets many requirements for nerve tissue quality and donor site morbidity and has become the standard autogenous graft for bridging large upper-extremity nerve gaps. Through a longitudinal incision or sequential small transverse incisions, up to 40 cm of nerve can be harvested from each leg.[64] The resulting sensory loss over the lateral aspect of the foot is not inconsequential; careful preoperative counseling is necessary to avoid postoperative disappointments. Blocking the nerve preoperatively with local anesthetic is very helpful in illustrating the resultant defect to the patient. In addition to the expected sensory loss, neuroma symptoms can produce morbidity.[65]

In the forearm, cutaneous nerve branches are available as graft material. Preoperative counseling and local anesthetic blocks to reproduce the donor defect are particularly useful here. The medial antebrachial cutaneous nerve (MACN) may be harvested and provides up to 10 cm of graft.[66] The resultant sensory deficit lies along the medial aspect of the mid-forearm.

The lateral antebrachial cutaneous nerve provides significantly more graft material than the MACN does -- up to 20 cm.[67,68,69] However, the resultant sensory loss along the lateral aspect of the forearm can extend onto the thenar area, making it undesirable for median nerve defects in general and thumb digital nerve injuries in particular.

The posterior interosseous nerve may be harvested at the wrist level and yields approximately 3.5 cm of graft material. The graft may be particularly useful in digital nerve defects,[63] and there is no donor morbidity from sensory loss.

The use of vascularized nerve grafts provides several potential advantages. The initial period of ischemia (2 to 3 days) after nonvascularized grafting is avoided, the necessity for revascularization via the recipient bed (which may be severely scarred and poorly vascularized) is eliminated, and larger sizes of nerve tissue (in cross section) may be used as graft without the problems of central necrosis. Table 6 lists donor nerves with a predictable arterial supply.

There is experimental evidence that vascularized nerve grafting can produce superior outcomes, though conclusive evidence is still lacking. Clinical series reported superior results with vascularized nerve grafts, though none had control groups and follow-up was frequently limited.[71,72,73,74,75,76] As more clinical follow-up becomes available, the indications for this technique may expand. The most compelling present indication is grafting in a severely scarred tissue bed.[71] Situations where transfer of large nerve trunks is desirable and feasible (eg, brachial plexus reconstruction using the ulnar nerve) may benefit from this technique, as well.

Ease of harvest and frequently perfect size match make autologous vein a predictable material for use in bridging nerve defects. Of course, the advantage of negligible donor morbidity must be offset by acceptable clinical results. A consideration of nerve regeneration biology suggests the ideal peripheral nerve for this technique would be small in caliber, motor or sensory only, and have a limited end-organ target area. The technique is reported in clinical studies for digital nerve repair.[78,79] Superiority over conventional nerve grafting has not been established. However, as our understanding of nerve regeneration through hollow tubes improves in general, indications may expand.

The use of allograft nerve material is particularly appealing because of its available quantity and lack of donor site morbidity. However, the risks of immunosuppression required to maintain Schwann cell viability limit clinical implementation of this method. In animal models, if continuous immunosuppression is used and the Schwann cell population in the graft survives, then regeneration equivalent to autograft can be expected.[80,81] Future improvements in immunosuppression may expand the use of allografts, but at present, they are not indicated in clinical practice.

Bridging nerve gaps with a hollow tube has been considered for over a century, utilizing a vast array of materials. As our understanding of nerve regeneration biology has improved, the conduits for regeneration have been refined considerably. The ideal conduit would allow inflow of supportive local nutrient factors but prevent escape of substances supportive of regeneration inside the tube. Ultimately, conduits filled with neurotrophic substances that are resorbable over appropriate periods may be available. Lundborg et al[82] reported a prospective clinical series evaluating median and ulnar nerve lesions in the forearm treated by conventional nerve suture or tubulation. Similar outcomes were found in the two groups. Further clinical trials are needed before the technique can be advocated for routine use.

Nerve Lesions in Continuity

Nerve lesions in continuity are also called a "neuroma in continuity." This clinical situation presents unique challenges to the surgeon managing peripheral nerve injury. The goal of management is the reconstruction of nonfunctioning neural elements without compromise of existing function. Regeneration failure can occur in a wide variety of clinical situations, including that following nerve repair. However, most commonly, crush injury, stretch injury (as may be seen with certain fractures), or gunshot wounds leave the nerve in continuity, but injured to some degree. The progress of nerve recovery can be followed clinically by assessment of functional -- both sensory and motor -- recovery. In addition, an advancing Tinel's sign is followed. After regeneration commences, the advancing axons progress approximately 1 mm/day. This information, coupled with a thorough understanding of the local peripheral nerve anatomy, allows the clinician to predict recovery. Partial recovery, anomalous innervation, or regeneration across long segments of nerve without branching (such as in the forearm) can challenge even the most careful observer.

When clinical progress is not proceeding as expected, electrodiagnostic studies can be useful in identifying regeneration before it is evident by examination. Electromyography provides specific information about muscle degeneration. Information gained may obviate the need for surgical treatment of the lesion and may avoid the situation in which exploration is delayed so long that end-organ degeneration occurs. If partial recovery is occurring, further management decisions are based on the critical nature of missing functions. When motor recovery has occurred but sensory return is lacking, exploration and intraoperative recordings can be done with a peripheral nerve stimulator, available in most operating rooms. Mackinnon[83] has described the intraoperative management sequence in detail. In brief, functioning motor fascicles are identified and excluded, allowing section and reconstruction of the injured sensory fascicles.

When sensory recovery is present but motor function is deficient, nerve-to-nerve recording is required. Specialized equipment for this process is not commonly available. In this situation, tendon transfers or referral to centers familiar with the technique may be appropriate. Happel and Kline[84] describe the intraoperative technique in detail.

Intraoperative testing, in general, identifies functioning fascicles before end-organ innervation. This information correlates well with eventual function and can therefore dependably identify fascicles that may be reconstructed.[85]

Aftercare and Rehabilitation

Postoperative management after nerve repair or reconstruction is directed toward wound healing, maintaining joint mobility, and reestablishing longitudinal excursion of the nerve. Repairs are immobilized for approximately 3 weeks. Adjacent joints are splinted in a safe position. Extremes of positioning are not indicated to allow repair without grafting, as discussed in the introductory section on nerve grafting.[86] After digital nerve repair, a careful intraoperative assessment of tension on the repair site, where the metacarpophalangeal (MP) joints are held in flexion and the interphalangeal joints in extension, provides critical information concerning early postoperative motion after tendon repair. Splinting for specific nerve injuries should prevent contracture during the months required for regeneration. After ulnar nerve repair, blocking the MP joints in 30° of flexion allows active interphalangeal motion but prevents hyperextension deformity at the MP joints. Abduction splinting prevents contractures of the first web space when thumb abduction is lost.

Sensory Reeducation
After nerve regeneration, a new and confusing set of signals is relayed from the hand to the brain. Innervation density is significantly reduced. Imperfect topographic specificity results in axon regeneration to new locations. For example, after median nerve repair, axons once destined for the middle finger may now innervate the palm. In addition, end-organ innervation is significantly altered. The resultant signal to the brain from sensory stimulation may be nearly unrecognizable. Sensory reeducation is designed to help the patient recognize new input in a useful manner. The ability to change cortical maps of sensory input and alter them to allow accurate identification of new sensory input is called cortical plasticity. Children are particularly adept at this process, which probably contributes greatly to their improved outcome after peripheral nerve injury.

Sensory reeducation is carried out in three stages: desensitization, early-phase discrimination and localization, and late-phase discrimination and tactile gnosis.[87] Initial efforts are directed toward helping the patient understand the potential risks present with a lack of protective sensation. As early recovery occurs, desensitization is accomplished by a program of graded stimuli, which gradually decreases unpleasant stimuli and builds tolerance for increasing levels of stimulus.

When a 30-cps tuning fork can be perceived in the palm, early-phase discrimination and localization begins. During this stage, the patient is taught to distinguish between static and moving touch. In addition, false localization of stimuli is addressed. Sensory stimuli are presented with and without visual clues. Once moving and constant touch can be dependably identified, late-phase training begins.

The goal of late-phase training is the reestablishment of tactile gnosis. Tactile gnosis describes the hand's unique ability to "see" an object and to provide extraordinary detail concerning its shape, texture, and temperature.[88] Objects that differ greatly in size, shape, and texture are presented sequentially to the patient. As perception improves, increasingly complex objects are used.

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