Disclosure History of the Procedure: Paul of Aegina (625-690) was the first to describe approximation of the nerve ends with wound closure. Hueter (1871, 1873) introduced the concept of primary epineurial nerve suture, and Nelaton described secondary nerve repair in 1864. Even at an early time, the idea of decreasing tension on the nerve suture was important. In 1882, Mikulicz described sutures that reduced tension, and Loebke described bone shortening to decrease nerve tension in 1884. In 1876, Albert described grafting nerve gaps. A great deal of information regarding the evaluation and treatment of traumatic nerve injuries came with the experience in wartime injuries. Problem: Loss of motor function, sensory function, or both may result from an injury to a peripheral nerve. Frequency: Limited reported data are available to determine incidence. In North America, data taken from a trauma population in Canada revealed that approximately 2-3% of patients had a major nerve injury. In New South Wales, Australia, 2% of patients were reported to have a major nerve injury. Etiology: Peripheral nerve injuries may occur due to trauma (eg, a blunt or penetrating wound, trauma) or acute compression. Pathophysiology: Injury may result in demyelination or axonal degeneration. Clinically, both demyelination and axonal degeneration result in disruption of the sensory and/or motor function of the injured nerve. Recovery of function occurs with remyelination and with axonal regeneration and reinnervation of the sensory receptors, muscle end plates, or both. Clinical: The clinical appearance of an injured nerve depends on the nerve affected. Injury to a motor nerve results in a loss of muscle function, and injury to a sensory nerve results in a loss of sensation to the affected nerve's sensory distribution and/or neuromatous or causalgia pain. Classification of nerve injury has been described by Seddon in 1943 and by Sunderland in 1951. The classification of nerve injury described by Seddon comprised neurapraxia, axonotmesis, and neurotmesis. Sunderland expanded this classification system to 5 degrees of nerve injury. A first-degree injury or neurapraxia involves a temporary conduction block with demyelination of the nerve at the site of injury. Electrodiagnostic study results are normal above and below the level of injury, and no denervation muscle changes are present. No Tinel sign is present. Once the nerve has remyelinated at that area, complete recovery occurs. Recovery may take up to 12 weeks. A second-degree injury or axonotmesis results from a more severe trauma or compression. This causes Wallerian degeneration distal to the level of injury and proximal axonal degeneration to at least the next node of Ranvier. In more severe traumatic injuries, the proximal degeneration may extend beyond the next node of Ranvier. Electrodiagnostic studies demonstrate denervation changes in the affected muscles, and in cases of reinnervation, motor unit potentials (MUPs) are present. Axonal regeneration occurs at the rate of 1 mm/d or 1 in/mo and can be monitored with an advancing Tinel sign. The endoneurial tubes remain intact, and, therefore, recovery is complete with axons reinnervating their original motor and sensory targets. A third-degree injury was introduced by Sunderland to describe an injury more severe than second-degree injury. Similar to a second-degree injury, Wallerian degeneration occurs, and electrodiagnostic studies demonstrate denervation changes with fibrillations in the affected muscles. In cases of reinnervation, MUPs are present. Regeneration occurs at 1 mm/d, and progress may be monitored with an advancing Tinel sign. However, with the increased severity of the injury, the endoneurial tubes are not intact, and regenerating axons therefore may not reinnervate their original motor and sensory targets. The pattern of recovery is mixed and incomplete. Reinnervation occurs only if sensory fibers reach their sensory end organs and motor fibers reach their muscle targets. Even within a sensory nerve, recovery can be mismatched if sensory fibers reinnervate a different sensory area within the nerve's sensory distribution. If the muscle target is a long distance from the site of injury, nerve regeneration may occur, but the muscle may not be completely reinnervated due to the long period of denervation. A fourth-degree injury results in a large area of scar at the site of nerve injury and precludes any axons from advancing distal to the level of nerve injury. Electrodiagnostic studies reveal denervation changes in the affected muscles, and no MUPs are present. A Tinel sign is noted at the level of the injury, but it does not advance beyond that level. No improvement in function is noted, and the patient requires surgery to restore neural continuity, thus permitting axonal regeneration and motor and sensory reinnervation. A fifth-degree injury is a complete transection of the nerve. Similar to a fourth-degree injury, it requires surgery to restore neural continuity. Electrodiagnostic findings are the same as those for a fourth-degree injury. A sixth-degree injury was introduced by Mackinnon to describe a mixed nerve injury that combines the other degrees of injury. This commonly occurs when some fascicles of the nerve are working normally while other fascicles may be recovering, and other fascicles may require surgical intervention to permit axonal regeneration.
Indications for surgery are as follows:
Relevant Anatomy: Nerve is composed of neural and connective tissue. In myelinated axons, each nerve fiber is surrounded by the endoneurium. Groups of nerve fibers are surrounded by the perineurium to form fascicles, and groups of fascicles are surrounded by the internal and external epineurium. Knowledge of motor and sensory fascicular topography within the nerve is essential to ensure correct alignment of the motor and sensory fascicles. Contraindications: In contaminated or crush injuries, delayed reconstruction may be indicated. |
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Lab Studies:
Imaging Studies:
Other Tests:
Medical therapy: Initial therapy involves protection of the joints, including the surrounding ligaments and tendons, from further stress. Splints, slings, or both may be used in these cases. For example, a radial nerve injury results in a loss of wrist and finger extension, a wrist drop. A wrist-resting splint may be used to support the hand in a neutral wrist position and place the hand in a more functional position. In patients with brachial plexus nerve injuries, particularly when C5-6 is affected, continued downward stress at the glenohumeral joint may cause the glenohumeral joint to subluxate without the muscle support of the rotator cuff muscles. A sling is helpful to unload this joint, prevent complete shoulder dislocation, and decrease pain. Physical therapy is started in the early stages following nerve injury to maintain passive range of motion in the affected joints and to maintain muscle strength in the unaffected muscles. No definitive studies have been done to support the use of electrical muscle stimulation to prevent muscle degeneration. In cases of muscle denervation, galvanic direct current stimulation is necessary to elicit a muscle contraction. The risks of galvanic stimulation include a thermal burn beneath the electrodes. Because no studies have shown that external stimulation will stop total degeneration of the muscle fibers and/or neuromuscular junction, the authors do not believe that direct current stimulation is worth the risk of a thermal burn. If the nerve does not regenerate in time to reinnervate the muscle, there is no need to stimulate the muscle. With reinnervated muscle, it is theoretically possible to use alternating current stimulation. However, it is necessary to have a large number of reinnervated muscle fibers to stimulate the muscle with alternating current. The authors recommend exercise and biofeedback strategies to increase the strength of a reinnervated muscle. Surgical therapy: Lacerations In patients with neurologic deficits following a laceration, an operative procedure to explore the nerve should be performed as soon after injury as possible. With clean sharp injuries to the nerve, a direct repair is performed. With more crushing or avulsion injuries, the nerve ends are reapproximated so that motor and sensory topography can be aligned. The definitive reconstruction is done at 3 weeks or when the wound permits. Gunshot wounds Typically, gunshot wounds associated with neurologic deficit have good potential for neurological recovery. Thus, unless an associated vascular or bony problem is present, the patient with a neurologic deficit following a gunshot wound is managed conservatively and monitored with frequent clinical examinations. By 3 months following injury, if no evidence of clinical recovery or electrical recovery is noted on electrodiagnostic testing, surgical exploration is recommended. Closed injuries In patients with closed traction injuries, surgical intervention is recommended 3 months following nerve injury. These patients are reexamined both clinically and with electrodiagnostic studies. With no evidence of reinnervation clinically or electrically, surgical intervention is necessary. Preoperative details: With no clinical or electrodiagnostic evidence of recovery, surgical exploration is recommended. Preoperative sensory evaluation should include measurement of 2-point discrimination. In patients with no 2-point discrimination, light touch (Ten test) is used. In the Ten test, simultaneous light touch stimuli are applied to the affected area of sensory compromise and to the contralateral region, and the patient compares the sensation on a scale of 0-10. Motor assessment should include pinch and grip strength measurements and evaluation of individual muscle strength using the Medical Research Council (MRC) 0-5 grading scale when appropriate (M0 = no contraction; M1 = flicker contraction; M2 = muscle contraction with active motion with gravity eliminated; M3 = full range of motion against gravity; M4 = full range of motion against gravity with some resistance; M5 = full range of motion against gravity with maximum resistance for that muscle). Intraoperative details: Technique
Nerve repair Reconstruction of nerve continuity can be performed with direct repair. This is performed when the 2 ends of the nerve are directly coapted. This should be performed without tension. If the repair cannot be performed without tension, nerve grafting should be performed. If the adjacent joint must be flexed or extended to permit coaptation of the distal and proximal ends of the nerve, a nerve graft should be used. (With wrist flexion, the median nerve can be directly repaired; if it is under tension with a wrist neutral position, a nerve graft should be used.) Nerve graft In cases in which a gap is present between the proximal and distal end of the nerve, a nerve graft is recommended. The use of a donor nerve results in a sensory loss in the distribution of the donor nerve. This area of sensory loss becomes smaller over 1-3 years with collateral sprouting from the surrounding sensory nerves. In cases in which a large nerve gap is present, the sural nerve is used due to the large length of nerve graft material that can be obtained. The sural nerve can be harvested through one long incision or through multiple step incisions on the posterior calf. For shorter nerve gaps, the anterior branch of the medial antebrachial cutaneous (MABC) nerve is a good nerve graft donor because the donor site scar is minimal and the resultant sensory loss is on the anterior aspect of the forearm. The MABC nerve is especially useful for surgical reconstructions in the upper extremity because all of the incisions are located in the same extremity. The lateral antebrachial cutaneous nerve provides about 6 cm of nerve graft material, but the scar on the forearm is more noticeable than that on the inner upper arm for the MABC. Nerve transfer The concept of a nerve-to-nerve transfer permits a normal neighboring noncritical nerve to be coapted to the distal end of the injured nerve. This is particularly useful in cases in which a large nerve gap is present and/or for proximal nerve injuries. Postoperative details: The patient is immobilized in a bulky dressing for several days following surgery. The postoperative dressing (including the drain and pain pump) is removed 2-3 days following surgery. The area of nerve coaptation then is immobilized for a longer time postoperatively (nerve graft for 10-14 d, nerve repair for 3 wk), although the patient is instructed in range of motion exercises for the joints proximal and distal to the immobilized region. For example, a median nerve repair at the wrist would be immobilized with a wrist-resting splint, and the patient would continue with range of motion for the fingers, elbow, and shoulder. Following surgery, the patient is sent to the hand therapist, initially for the splint and then for exercises. Initially, the goals of therapy are to regain passive range of motion of the joints and soft tissues that have been immobilized. The patient should be instructed in exercises to maintain strength in the unaffected muscles. In the later stages, sensory and motor reeducation is recommended to maximize the outcome. Follow-up care: Initially, the patient is monitored for postoperative wound healing. After immobilization and once the patient regains full passive range of motion, the patient is monitored every few months to evaluate for evidence of reinnervation. With nerve regeneration, a Tinel sign progresses distally along the nerve. With muscle reinnervation, a muscle contraction is visible, and with sensory reinnervation, the patient responds to light touch. Depending on the level of injury, the patient may continue to progress for varying periods, distal injuries more quickly and proximal brachial plexus injuries for 2-3 years following surgery.
Complications of nerve surgery are similar to those of other surgeries and include infection, hematoma, seroma, and injury to surrounding structures, including vascular structures. Unique to nerve surgery is the possibility of downgrading function by further injuring the nerve, particularly in mixed nerve injuries.
With restoration of nerve continuity, axons may regenerate and, thus, reinnervate the motor end plates and sensory receptors. When the nerve injury is very proximal (ie, brachial plexus injury, sciatic nerve injury), nerve regeneration may not occur in sufficient time for muscle reinnervation. For example, in a lower trunk brachial plexus injury, reinnervation of the ulnar nerve intrinsic hand muscles is not possible due to the long period of muscle denervation because of the long distance necessary for nerve regeneration. However, if surgery is performed within 3-6 months following nerve injury, the patient is expected to recover use of most muscles, excluding muscles in the hand or foot in injuries at the trunk level or higher. Distal nerve transfers are used to recover distal extremity motor function.
The future in peripheral nerve injuries lies in maximizing motor and sensory recovery following nerve injury. Strategies to maintain the neuromuscular junction are important to permit muscle reinnervation following prolonged muscle denervation, in addition to decreasing injury to the cell body. In traumatic nerve injury with large nerve gaps, nerve allografts may be considered. However, because of the morbidity associated with immunosuppression, the use of the nerve allograft has been limited to otherwise unreconstructable injuries. Investigations to decrease the antigenicity of the allograft and/or induce tolerance to the nerve allograft are ongoing, and success in these investigations will permit the use of nerve allografts without immunosuppression.
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